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astrocyte functions or gain of abnormal effects to contribute to, or play primary roles in, disease processes, and there are now numerous examples of astrocyte contributions to clinical and pathological mechanisms [>>15<<, 52, 212, 224\u2013226, 237]." ; ns1:mentions . _:b6628351 rdf:type ns1:Context ; rdf:value "loss of normal astrocyte functions or gain of abnormal effects to contribute to, or play primary roles in, disease processes, and there are now numerous examples of astrocyte contributions to clinical and pathological mechanisms [15, >>52<<, 212, 224\u2013226, 237]." ; ns1:mentions . _:b6628352 rdf:type ns1:Context ; rdf:value "of normal astrocyte functions or gain of abnormal effects to contribute to, or play primary roles in, disease processes, and there are now numerous examples of astrocyte contributions to clinical and pathological mechanisms [15, 52, >>212<<, 224\u2013226, 237]." ; ns1:mentions . _:b6628353 rdf:type ns1:Context ; rdf:value "normal astrocyte functions or gain of abnormal effects to contribute to, or play primary roles in, disease processes, and there are now numerous examples of astrocyte contributions to clinical and pathological mechanisms [15, 52, 212, >>224<<\u2013226, 237]." ; ns1:mentions , . _:b6628354 rdf:type ns1:Context ; rdf:value "functions or gain of abnormal effects to contribute to, or play primary roles in, disease processes, and there are now numerous examples of astrocyte contributions to clinical and pathological mechanisms [15, 52, 212, 224\u2013226, >>237<<]. This article summarizes recent advances in (1) astrocyte functions in healthy tissue, (2) the gradations, mechanisms, functions, and effects of reactive astrogliosis, and (3) the appearance and potential roles of reactive astrocytes in" ; ns1:mentions . _:b6628355 rdf:type ns4:Section ; dc:title "astrocyte biology in healthy cns" ; ns4:contains _:b6628480 , _:b6628481 , _:b6628456 , _:b6628457 , _:b6628458 , _:b6628459 , _:b6628460 , _:b6628461 , _:b6628462 , _:b6628463 , _:b6628448 , _:b6628449 , _:b6628450 , _:b6628451 , _:b6628452 , _:b6628453 , _:b6628454 , _:b6628455 , _:b6628472 , _:b6628473 , _:b6628474 , _:b6628475 , _:b6628476 , _:b6628477 , _:b6628478 , _:b6628479 , _:b6628464 , _:b6628465 , _:b6628466 , _:b6628467 , _:b6628468 , _:b6628469 , _:b6628470 , _:b6628471 , _:b6628424 , _:b6628425 , _:b6628426 , _:b6628427 , _:b6628428 , _:b6628429 , _:b6628430 , _:b6628431 , _:b6628416 , _:b6628417 , _:b6628418 , _:b6628419 , _:b6628420 , _:b6628421 , _:b6628422 , _:b6628423 , _:b6628440 , _:b6628441 , _:b6628442 , _:b6628443 , _:b6628444 , _:b6628445 , _:b6628446 , _:b6628447 , _:b6628432 , _:b6628433 , _:b6628434 , _:b6628435 , _:b6628436 , _:b6628437 , _:b6628438 , _:b6628439 , _:b6628392 , _:b6628393 , _:b6628394 , _:b6628395 , _:b6628396 , _:b6628397 , _:b6628398 , _:b6628399 , _:b6628384 , _:b6628385 , _:b6628386 , _:b6628387 , _:b6628388 , _:b6628389 , _:b6628390 , _:b6628391 , _:b6628408 , _:b6628409 , _:b6628410 , _:b6628411 , _:b6628412 , _:b6628413 , _:b6628414 , _:b6628415 , _:b6628400 , _:b6628401 , _:b6628402 , _:b6628403 , _:b6628404 , _:b6628405 , _:b6628406 , _:b6628407 , _:b6628360 , _:b6628361 , _:b6628362 , _:b6628363 , _:b6628364 , _:b6628365 , _:b6628366 , _:b6628367 , _:b6628356 , _:b6628357 , _:b6628358 , _:b6628359 , _:b6628376 , _:b6628377 , _:b6628378 , _:b6628379 , _:b6628380 , _:b6628381 , _:b6628382 , _:b6628383 , _:b6628368 , _:b6628369 , _:b6628370 , _:b6628371 , _:b6628372 , _:b6628373 , _:b6628374 , _:b6628375 . _:b6628356 rdf:type ns1:Context ; rdf:value "b Two color fluorescence showing astrocytes in healthy mouse gray matter stained immunohistochemically for GFAP (red) as well as the transgene-derived reporter molecule GFP (green). Note that in these transgenic mice [>>95<<], GFP reporter is present in all of the fine processes of the protoplasmic astrocytes throughout the neuropil, whereas the GFAP is present only in the large stem astrocyte processes and endfeet (which appear yellow where green and red" ; ns1:mentions . _:b6628357 rdf:type ns1:Context ; rdf:value "Transgenic disruption of this reactive astrocyte barrier leads to widespread invasion of inflammatory cells away from perivascular clusters into CNS parenchyma during EAE [>>251<<]. d Two color brightfield staining showing human autopsy specimen with reactive astrocytes lining their processes along perivascular cuffs of inflammatory cells as if forming perivascular scar-like barriers similar to those observed in" ; ns1:mentions . _:b6628358 rdf:type ns1:Context ; rdf:value "showing human autopsy specimen with reactive astrocytes lining their processes along perivascular cuffs of inflammatory cells as if forming perivascular scar-like barriers similar to those observed in experimental animal models [>>251<<]. Scale bars a 3\u00A0\u03BCm, b 7.5\u00A0\u03BCm, c 15\u00A0\u03BCm, d 5" ; ns1:mentions . _:b6628359 rdf:type ns1:Context ; rdf:value "as a protein highly concentrated in old demyelinated plaques from multiple sclerosis patients and was then found to be associated immunohistochemically with reactive astrocytes in such plaques and in other pathological contexts [62, >>63<<]. In line with this original mode of identification, GFAP expression can be regarded as a sensitive and reliable marker that labels most, if not all, reactive astrocytes that are responding to CNS injuries (Fig." ; ns1:mentions . _:b6628360 rdf:type ns1:Context ; rdf:value "CNS tissue do not express detectable levels of GFAP and that GFAP expression by astrocytes exhibits both regional and local variability that is dynamically regulated by a large number of inter- and intra-cellular signaling molecules [>>226<<].Fig." ; ns1:mentions . _:b6628361 rdf:type ns1:Context ; rdf:value "GFAP is one of a family of intermediate filament proteins, including vimentin, nestin, and others, that serve largely cyto-architectural functions [>>179<<]. Studies in transgenic mice indicated that the expression of GFAP is not essential for the normal appearance and function of most astrocytes in healthy CNS of transgenic mice, but is essential for the process of reactive astrogliosis and" ; ns1:mentions . _:b6628362 rdf:type ns1:Context ; rdf:value "mice indicated that the expression of GFAP is not essential for the normal appearance and function of most astrocytes in healthy CNS of transgenic mice, but is essential for the process of reactive astrogliosis and glial scar formation [>>95<<, 179, 180]." ; ns1:mentions . _:b6628363 rdf:type ns1:Context ; rdf:value "indicated that the expression of GFAP is not essential for the normal appearance and function of most astrocytes in healthy CNS of transgenic mice, but is essential for the process of reactive astrogliosis and glial scar formation [95, >>179<<, 180]. There are different isoforms and splice variants of GFAP including GFAP \u03B1, \u03B2, \u03B3, \u03B4, and \u03BA, and these may be expressed in a heterogeneous manner in both healthy CNS and in pathological specimens including glioma, but the" ; ns1:mentions . _:b6628364 rdf:type ns1:Context ; rdf:value "that the expression of GFAP is not essential for the normal appearance and function of most astrocytes in healthy CNS of transgenic mice, but is essential for the process of reactive astrogliosis and glial scar formation [95, 179, >>180<<]. There are different isoforms and splice variants of GFAP including GFAP \u03B1, \u03B2, \u03B3, \u03B4, and \u03BA, and these may be expressed in a heterogeneous manner in both healthy CNS and in pathological specimens including glioma, but the differential" ; ns1:mentions . _:b6628365 rdf:type ns1:Context ; rdf:value "\u03B1, \u03B2, \u03B3, \u03B4, and \u03BA, and these may be expressed in a heterogeneous manner in both healthy CNS and in pathological specimens including glioma, but the differential distribution and roles of GFAP isoforms are only beginning to be studied [>>4<<, 20, 195]." ; ns1:mentions . _:b6628366 rdf:type ns1:Context ; rdf:value "\u03B2, \u03B3, \u03B4, and \u03BA, and these may be expressed in a heterogeneous manner in both healthy CNS and in pathological specimens including glioma, but the differential distribution and roles of GFAP isoforms are only beginning to be studied [4, >>20<<, 195]." ; ns1:mentions . _:b6628367 rdf:type ns1:Context ; rdf:value "\u03B3, \u03B4, and \u03BA, and these may be expressed in a heterogeneous manner in both healthy CNS and in pathological specimens including glioma, but the differential distribution and roles of GFAP isoforms are only beginning to be studied [4, 20, >>195<<]." ; ns1:mentions . _:b6628368 rdf:type ns1:Context ; rdf:value "1a) or expression of reporter proteins such as GFP or \u03B2-galactosidase (Fig.\u00A01b), or filling with fluorescent dyes [>>34<<]." ; ns1:mentions . _:b6628369 rdf:type ns1:Context ; rdf:value "Other molecular markers that have been used for immunohistochemical identification of astrocytes and reactive astrocytes include glutamine synthetase and S100\u03B2 [>>85<<, 165], but these molecules are not entirely exclusive to astrocytes." ; ns1:mentions . _:b6628370 rdf:type ns1:Context ; rdf:value "Other molecular markers that have been used for immunohistochemical identification of astrocytes and reactive astrocytes include glutamine synthetase and S100\u03B2 [85, >>165<<], but these molecules are not entirely exclusive to astrocytes." ; ns1:mentions . _:b6628371 rdf:type ns1:Context ; rdf:value "conducted large-scale genetic analysis of the astrocyte transcriptome in rodents and humans, and have identified large numbers of molecules enriched in astrocytes as compared with other neural cells such as neurons and oligodendrocytes [>>35<<, 129]. Such studies will provide a rich resource for identifying molecules for mechanistic analyses of functions and roles of astrocytes and reactive astrocytes." ; ns1:mentions . _:b6628372 rdf:type ns1:Context ; rdf:value "large-scale genetic analysis of the astrocyte transcriptome in rodents and humans, and have identified large numbers of molecules enriched in astrocytes as compared with other neural cells such as neurons and oligodendrocytes [35, >>129<<]. Such studies will provide a rich resource for identifying molecules for mechanistic analyses of functions and roles of astrocytes and reactive astrocytes." ; ns1:mentions . _:b6628373 rdf:type ns1:Context ; rdf:value "the expression of reporter molecules such as GFP (green fluorescent protein) to astrocytes and whose identification by immunohistochemistry may provide a sensitive chemical marker for most if not all astrocytes in healthy tissue [>>15<<]." ; ns1:mentions . _:b6628374 rdf:type ns1:Context ; rdf:value "in gray matter, such that only the most distal tips of processes from individual astrocytes interdigitate with one another and thereby provide the substrate for formation of the gap junctions detected at the ultrastructural level [>>34<<, 91, 162, 172]. Similar individual astrocyte domains appear likely to exist in white matter, but this has not yet been as extensively reported on." ; ns1:mentions . _:b6628375 rdf:type ns1:Context ; rdf:value "in gray matter, such that only the most distal tips of processes from individual astrocytes interdigitate with one another and thereby provide the substrate for formation of the gap junctions detected at the ultrastructural level [34, >>91<<, 162, 172]. Similar individual astrocyte domains appear likely to exist in white matter, but this has not yet been as extensively reported on." ; ns1:mentions . _:b6628376 rdf:type ns1:Context ; rdf:value "gray matter, such that only the most distal tips of processes from individual astrocytes interdigitate with one another and thereby provide the substrate for formation of the gap junctions detected at the ultrastructural level [34, 91, >>162<<, 172]. Similar individual astrocyte domains appear likely to exist in white matter, but this has not yet been as extensively reported on." ; ns1:mentions . _:b6628377 rdf:type ns1:Context ; rdf:value "matter, such that only the most distal tips of processes from individual astrocytes interdigitate with one another and thereby provide the substrate for formation of the gap junctions detected at the ultrastructural level [34, 91, 162, >>172<<]. Similar individual astrocyte domains appear likely to exist in white matter, but this has not yet been as extensively reported on." ; ns1:mentions . _:b6628378 rdf:type ns1:Context ; rdf:value "In hippocampus or cortex many finely branching processes from a single astrocyte are estimated to contact several hundred dendrites from multiple neurons and to envelope 100,000 or more synapses [>>34<<, 91, 172]." ; ns1:mentions . _:b6628379 rdf:type ns1:Context ; rdf:value "In hippocampus or cortex many finely branching processes from a single astrocyte are estimated to contact several hundred dendrites from multiple neurons and to envelope 100,000 or more synapses [34, >>91<<, 172]. It is also noteworthy that human astrocytes are larger, structurally more complex, and more diverse than astrocytes in rodents [170]." ; ns1:mentions . _:b6628380 rdf:type ns1:Context ; rdf:value "In hippocampus or cortex many finely branching processes from a single astrocyte are estimated to contact several hundred dendrites from multiple neurons and to envelope 100,000 or more synapses [34, 91, >>172<<]. It is also noteworthy that human astrocytes are larger, structurally more complex, and more diverse than astrocytes in rodents [170]." ; ns1:mentions . _:b6628381 rdf:type ns1:Context ; rdf:value "It is also noteworthy that human astrocytes are larger, structurally more complex, and more diverse than astrocytes in rodents [>>170<<]." ; ns1:mentions . _:b6628382 rdf:type ns1:Context ; rdf:value "Astrocytes express potassium and sodium channels and can exhibit evoked inward currents, but unlike neurons, astrocytes do not \u2018fire\u2019 or propagate action potentials along their processes [>>162<<, 212]. However, this does not mean that astrocytes are physiologically \u2018silent\u2019." ; ns1:mentions . _:b6628383 rdf:type ns1:Context ; rdf:value "Astrocytes express potassium and sodium channels and can exhibit evoked inward currents, but unlike neurons, astrocytes do not \u2018fire\u2019 or propagate action potentials along their processes [162, >>212<<]. However, this does not mean that astrocytes are physiologically \u2018silent\u2019. Astrocytes exhibit regulated increases in intracellular calcium concentration [Ca++]i that represent a form of astrocyte excitability [39, 46]." ; ns1:mentions . _:b6628384 rdf:type ns1:Context ; rdf:value "Astrocytes exhibit regulated increases in intracellular calcium concentration [Ca++]i that represent a form of astrocyte excitability [>>39<<, 46]. A large body of evidence is now available that these regulated increases in astrocyte [Ca++]i are of functional significance in astrocyte\u2013astrocyte as well as in astrocyte\u2013neuron intercellular communication. Astrocyte [Ca++]i" ; ns1:mentions . _:b6628385 rdf:type ns1:Context ; rdf:value "Astrocytes exhibit regulated increases in intracellular calcium concentration [Ca++]i that represent a form of astrocyte excitability [39, >>46<<]. A large body of evidence is now available that these regulated increases in astrocyte [Ca++]i are of functional significance in astrocyte\u2013astrocyte as well as in astrocyte\u2013neuron intercellular communication. Astrocyte [Ca++]i elevations" ; ns1:mentions . _:b6628386 rdf:type ns1:Context ; rdf:value "during neuronal activity, (3) elicit the release from astrocytes of transmitters such as glutamate into the extracellular space and thereby trigger receptor mediated currents in neurons, and (4) be propagated to neighboring astrocytes [>>89<<, 162, 182, 215, 249]. Evidence that calcium signaling enables astrocytes to play a direct role in synaptic transmission is discussed below." ; ns1:mentions . _:b6628387 rdf:type ns1:Context ; rdf:value "neuronal activity, (3) elicit the release from astrocytes of transmitters such as glutamate into the extracellular space and thereby trigger receptor mediated currents in neurons, and (4) be propagated to neighboring astrocytes [89, >>162<<, 182, 215, 249]. Evidence that calcium signaling enables astrocytes to play a direct role in synaptic transmission is discussed below." ; ns1:mentions . _:b6628388 rdf:type ns1:Context ; rdf:value "activity, (3) elicit the release from astrocytes of transmitters such as glutamate into the extracellular space and thereby trigger receptor mediated currents in neurons, and (4) be propagated to neighboring astrocytes [89, 162, 182, >>215<<, 249]. Evidence that calcium signaling enables astrocytes to play a direct role in synaptic transmission is discussed below." ; ns1:mentions . _:b6628389 rdf:type ns1:Context ; rdf:value "(3) elicit the release from astrocytes of transmitters such as glutamate into the extracellular space and thereby trigger receptor mediated currents in neurons, and (4) be propagated to neighboring astrocytes [89, 162, 182, 215, >>249<<]. Evidence that calcium signaling enables astrocytes to play a direct role in synaptic transmission is discussed below." ; ns1:mentions . _:b6628390 rdf:type ns1:Context ; rdf:value "2a) formed by connexins, and that the gap junctional coupling of astrocytes into multicellular networks may play a role in both normal function and CNS disorders [>>162<<, 212]." ; ns1:mentions . _:b6628391 rdf:type ns1:Context ; rdf:value "2a) formed by connexins, and that the gap junctional coupling of astrocytes into multicellular networks may play a role in both normal function and CNS disorders [162, >>212<<]." ; ns1:mentions . _:b6628392 rdf:type ns1:Context ; rdf:value "Molecular boundaries formed by astrocytes take part in guiding the migration of developing axons and certain neuroblasts [>>186<<]. In addition, substantive evidence is accumulating that astrocytes are essential for the formation and function of developing synapses by releasing molecular signals such as thrombospondin [15, 43, 243]. Astrocytes appear also to" ; ns1:mentions . _:b6628393 rdf:type ns1:Context ; rdf:value "In addition, substantive evidence is accumulating that astrocytes are essential for the formation and function of developing synapses by releasing molecular signals such as thrombospondin [>>15<<, 43, 243]." ; ns1:mentions . _:b6628394 rdf:type ns1:Context ; rdf:value "In addition, substantive evidence is accumulating that astrocytes are essential for the formation and function of developing synapses by releasing molecular signals such as thrombospondin [15, >>43<<, 243]. Astrocytes appear also to influence developmental synaptic pruning by releasing signals that induce expression of complement C1q in synapses and thereby tag them for elimination by microglia [15, 230]. As regards the development of" ; ns1:mentions . _:b6628395 rdf:type ns1:Context ; rdf:value "In addition, substantive evidence is accumulating that astrocytes are essential for the formation and function of developing synapses by releasing molecular signals such as thrombospondin [15, 43, >>243<<]. Astrocytes appear also to influence developmental synaptic pruning by releasing signals that induce expression of complement C1q in synapses and thereby tag them for elimination by microglia [15, 230]. As regards the development of" ; ns1:mentions . _:b6628396 rdf:type ns1:Context ; rdf:value "Astrocytes appear also to influence developmental synaptic pruning by releasing signals that induce expression of complement C1q in synapses and thereby tag them for elimination by microglia [>>15<<, 230]. As regards the development of white matter, the loss or dysfunction of astrocyte connexins and gap junctions leads to dysmelination [131]." ; ns1:mentions . _:b6628397 rdf:type ns1:Context ; rdf:value "Astrocytes appear also to influence developmental synaptic pruning by releasing signals that induce expression of complement C1q in synapses and thereby tag them for elimination by microglia [15, >>230<<]. As regards the development of white matter, the loss or dysfunction of astrocyte connexins and gap junctions leads to dysmelination [131]." ; ns1:mentions . _:b6628398 rdf:type ns1:Context ; rdf:value "As regards the development of white matter, the loss or dysfunction of astrocyte connexins and gap junctions leads to dysmelination [>>131<<]." ; ns1:mentions . _:b6628399 rdf:type ns1:Context ; rdf:value "that astrocytes produce and release various molecular mediators, such prostaglandins (PGE), nitric oxide (NO), and arachidonic acid (AA), that can increase or decrease CNS blood vessel diameter and blood flow in a coordinated manner [>>86<<, 102]. Moreover, astrocytes may be primary mediators of changes in local CNS blood flow in response to changes in neuronal activity [112]." ; ns1:mentions . _:b6628400 rdf:type ns1:Context ; rdf:value "astrocytes produce and release various molecular mediators, such prostaglandins (PGE), nitric oxide (NO), and arachidonic acid (AA), that can increase or decrease CNS blood vessel diameter and blood flow in a coordinated manner [86, >>102<<]. Moreover, astrocytes may be primary mediators of changes in local CNS blood flow in response to changes in neuronal activity [112]." ; ns1:mentions . _:b6628401 rdf:type ns1:Context ; rdf:value "Moreover, astrocytes may be primary mediators of changes in local CNS blood flow in response to changes in neuronal activity [>>112<<]. Astrocytes have processes in contact with both blood vessels and synapses (Fig.\u00A02a). Via these contacts, astrocytes titrate blood flow in relation to levels of synaptic activity, as demonstrated recently in the visual cortex where fMRI" ; ns1:mentions . _:b6628402 rdf:type ns1:Context ; rdf:value "titrate blood flow in relation to levels of synaptic activity, as demonstrated recently in the visual cortex where fMRI detected changes in blood flow in response to visual stimuli were shown to be dependent on astrocyte function [>>211<<, 260]." ; ns1:mentions . _:b6628403 rdf:type ns1:Context ; rdf:value "titrate blood flow in relation to levels of synaptic activity, as demonstrated recently in the visual cortex where fMRI detected changes in blood flow in response to visual stimuli were shown to be dependent on astrocyte function [211, >>260<<]." ; ns1:mentions . _:b6628404 rdf:type ns1:Context ; rdf:value "Astrocyte processes envelop essentially all synapses [>>27<<, 183] and exert essential functions in maintaining the fluid, ion, pH, and transmitter homeostasis of the synaptic interstitial fluid in a manner that is critical for healthy synaptic transmission (Fig." ; ns1:mentions . _:b6628405 rdf:type ns1:Context ; rdf:value "Astrocyte processes are rich in the aquaporin 4 (AQP4) water channel and in transporters for the uptake of K+ [>>212<<, 220, 264]." ; ns1:mentions . _:b6628406 rdf:type ns1:Context ; rdf:value "Astrocyte processes are rich in the aquaporin 4 (AQP4) water channel and in transporters for the uptake of K+ [212, >>220<<, 264]. Astrocyte membranes have different means of proton shuttling, including the Na+/H+ exchanger, bicarbonate transporters, monocarboxylic acid transporters, and the vacuolar-type proton ATPase [168]. AQP4 water channels are densely" ; ns1:mentions . _:b6628407 rdf:type ns1:Context ; rdf:value "Astrocyte processes are rich in the aquaporin 4 (AQP4) water channel and in transporters for the uptake of K+ [212, 220, >>264<<]. Astrocyte membranes have different means of proton shuttling, including the Na+/H+ exchanger, bicarbonate transporters, monocarboxylic acid transporters, and the vacuolar-type proton ATPase [168]. AQP4 water channels are densely" ; ns1:mentions . _:b6628408 rdf:type ns1:Context ; rdf:value "Astrocyte membranes have different means of proton shuttling, including the Na+/H+ exchanger, bicarbonate transporters, monocarboxylic acid transporters, and the vacuolar-type proton ATPase [>>168<<]. AQP4 water channels are densely clustered along astrocyte processes that contact blood vessels and play a critical role in regulating fluid homeostasis in healthy CNS and play roles in both vasogenic and cytotoxic edema as discussed" ; ns1:mentions . _:b6628409 rdf:type ns1:Context ; rdf:value "synapses also play essential roles in transmitter homeostasis by expressing high levels of transporters for neurotransmitters such as glutamate, GABA, and glycine that serve to clear the neurotransmitters from the synaptic space [205, >>212<<]. After uptake into astrocytes, the transmitters are converted by enzymes such as glutamine synthetase into precursors such as glutamine and recycled back to synapses for reconversion into active transmitters (Fig." ; ns1:mentions . _:b6628410 rdf:type ns1:Context ; rdf:value "Networks of astrocytes linked together by gap junctions are thought to be able to rapidly dissipate small molecules such as potassium and glutamate and prevent their potentially detrimental accumulation (Fig.\u00A02a) [>>212<<]." ; ns1:mentions . _:b6628411 rdf:type ns1:Context ; rdf:value "There is now steadily accumulating evidence that astrocytes play direct roles in synaptic transmission through the regulated release of synaptically active molecules including glutamate, purines (ATP and adenosine), GABA, and D-serine [>>89<<, 162, 182, 215]." ; ns1:mentions . _:b6628412 rdf:type ns1:Context ; rdf:value "is now steadily accumulating evidence that astrocytes play direct roles in synaptic transmission through the regulated release of synaptically active molecules including glutamate, purines (ATP and adenosine), GABA, and D-serine [89, >>162<<, 182, 215]." ; ns1:mentions . _:b6628413 rdf:type ns1:Context ; rdf:value "accumulating evidence that astrocytes play direct roles in synaptic transmission through the regulated release of synaptically active molecules including glutamate, purines (ATP and adenosine), GABA, and D-serine [89, 162, 182, >>215<<]. The release of such gliotransmitters occurs in response to changes in neuronal synaptic activity, involves astrocyte excitability as reflected by increases in astrocyte [Ca++]i, and can alter neuronal excitability [89, 162, 182, 215]." ; ns1:mentions . _:b6628414 rdf:type ns1:Context ; rdf:value "The release of such gliotransmitters occurs in response to changes in neuronal synaptic activity, involves astrocyte excitability as reflected by increases in astrocyte [Ca++]i, and can alter neuronal excitability [>>89<<, 162, 182, 215]." ; ns1:mentions . _:b6628415 rdf:type ns1:Context ; rdf:value "The release of such gliotransmitters occurs in response to changes in neuronal synaptic activity, involves astrocyte excitability as reflected by increases in astrocyte [Ca++]i, and can alter neuronal excitability [89, >>162<<, 182, 215]." ; ns1:mentions . _:b6628416 rdf:type ns1:Context ; rdf:value "The release of such gliotransmitters occurs in response to changes in neuronal synaptic activity, involves astrocyte excitability as reflected by increases in astrocyte [Ca++]i, and can alter neuronal excitability [89, 162, 182, >>215<<]. Such evidence has given rise to the \u2018tripartite synapse\u2019 hypothesis, which posits that astrocytes play direct and interactive roles with neurons during synaptic activity in a manner that is essential for information processing by neural" ; ns1:mentions . _:b6628417 rdf:type ns1:Context ; rdf:value "has given rise to the \u2018tripartite synapse\u2019 hypothesis, which posits that astrocytes play direct and interactive roles with neurons during synaptic activity in a manner that is essential for information processing by neural circuits [>>5<<, 89, 182]." ; ns1:mentions . _:b6628418 rdf:type ns1:Context ; rdf:value "has given rise to the \u2018tripartite synapse\u2019 hypothesis, which posits that astrocytes play direct and interactive roles with neurons during synaptic activity in a manner that is essential for information processing by neural circuits [5, >>89<<, 182]." ; ns1:mentions . _:b6628419 rdf:type ns1:Context ; rdf:value "As discussed above, molecular mechanisms have been identified through which astrocytes play a role in the formation, maintenance, and pruning of synapses during development [>>15<<, 43, 230]." ; ns1:mentions . _:b6628420 rdf:type ns1:Context ; rdf:value "As discussed above, molecular mechanisms have been identified through which astrocytes play a role in the formation, maintenance, and pruning of synapses during development [15, >>43<<, 230]. Such mechanisms may also provide astrocytes with the means of exerting powerful influences on synaptic remodeling and pruning in the healthy adult CNS or in response to CNS disorders [15]. Cytokines such as tumor necrosis alpha" ; ns1:mentions . _:b6628421 rdf:type ns1:Context ; rdf:value "As discussed above, molecular mechanisms have been identified through which astrocytes play a role in the formation, maintenance, and pruning of synapses during development [15, 43, >>230<<]. Such mechanisms may also provide astrocytes with the means of exerting powerful influences on synaptic remodeling and pruning in the healthy adult CNS or in response to CNS disorders [15]. Cytokines such as tumor necrosis alpha (TNF\u03B1)" ; ns1:mentions . _:b6628422 rdf:type ns1:Context ; rdf:value "Such mechanisms may also provide astrocytes with the means of exerting powerful influences on synaptic remodeling and pruning in the healthy adult CNS or in response to CNS disorders [>>15<<]. Cytokines such as tumor necrosis alpha (TNF\u03B1) have been shown to influence homeostatic synaptic scaling by inducing the insertion of AMPA receptors at post-synaptic membranes [229]. Although it is not certain whether astrocytes or" ; ns1:mentions . _:b6628423 rdf:type ns1:Context ; rdf:value "Cytokines such as tumor necrosis alpha (TNF\u03B1) have been shown to influence homeostatic synaptic scaling by inducing the insertion of AMPA receptors at post-synaptic membranes [>>229<<]. Although it is not certain whether astrocytes or microglia are primary sources of TNF\u03B1 in the CNS in vivo, the effects on synaptic function of astrocyte-derived growth factors and cytokines warrant further study. Astrocytes are also" ; ns1:mentions . _:b6628424 rdf:type ns1:Context ; rdf:value "Astrocytes are also sources of neuroactive steroids (neurosteroids), including estradiol, progesterone and various intermediaries and metabolites that can have synaptic effects, particularly at GABAA receptors [>>80<<]." ; ns1:mentions . _:b6628425 rdf:type ns1:Context ; rdf:value "Although it was known for many years that astrocytes are the principal storage sites of glycogen granules in the CNS and that the greatest accumulation of astrocytic glycogen occurs in areas of high synaptic density [183, >>184<<], the functional contribution of these stores was originally discounted [27]." ; ns1:mentions . _:b6628426 rdf:type ns1:Context ; rdf:value "storage sites of glycogen granules in the CNS and that the greatest accumulation of astrocytic glycogen occurs in areas of high synaptic density [183, 184], the functional contribution of these stores was originally discounted [>>27<<]. Compelling evidence now demonstrates that astrocytic glycogen utilization can sustain neuronal activity during hypoglycemia and during periods of high neuronal activity [27, 231]." ; ns1:mentions . _:b6628427 rdf:type ns1:Context ; rdf:value "Compelling evidence now demonstrates that astrocytic glycogen utilization can sustain neuronal activity during hypoglycemia and during periods of high neuronal activity [>>27<<, 231]. In this regard, it is noteworthy that astrocyte glycogen content can be modulated by transmitters such as glutamate [27] and that glucose metabolites can be passed across gap junctions in a manner that is regulated by glutamate and" ; ns1:mentions . _:b6628428 rdf:type ns1:Context ; rdf:value "Compelling evidence now demonstrates that astrocytic glycogen utilization can sustain neuronal activity during hypoglycemia and during periods of high neuronal activity [27, >>231<<]. In this regard, it is noteworthy that astrocyte glycogen content can be modulated by transmitters such as glutamate [27] and that glucose metabolites can be passed across gap junctions in a manner that is regulated by glutamate and" ; ns1:mentions . _:b6628429 rdf:type ns1:Context ; rdf:value "In this regard, it is noteworthy that astrocyte glycogen content can be modulated by transmitters such as glutamate [>>27<<] and that glucose metabolites can be passed across gap junctions in a manner that is regulated by glutamate and neuronal activity [200]." ; ns1:mentions . _:b6628430 rdf:type ns1:Context ; rdf:value "it is noteworthy that astrocyte glycogen content can be modulated by transmitters such as glutamate [27] and that glucose metabolites can be passed across gap junctions in a manner that is regulated by glutamate and neuronal activity [>>200<<]. Other lines of evidence indicate that during hypoglycemia, astrocyte glycogen breaks down to lactate that is transferred to adjacent neural elements (both synapses in gray matter and axons in white matter) where it is used aerobically" ; ns1:mentions . _:b6628431 rdf:type ns1:Context ; rdf:value "of evidence indicate that during hypoglycemia, astrocyte glycogen breaks down to lactate that is transferred to adjacent neural elements (both synapses in gray matter and axons in white matter) where it is used aerobically as fuel [>>27<<, 28, 181, 252]." ; ns1:mentions . _:b6628432 rdf:type ns1:Context ; rdf:value "of evidence indicate that during hypoglycemia, astrocyte glycogen breaks down to lactate that is transferred to adjacent neural elements (both synapses in gray matter and axons in white matter) where it is used aerobically as fuel [27, >>28<<, 181, 252]." ; ns1:mentions . _:b6628433 rdf:type ns1:Context ; rdf:value "indicate that during hypoglycemia, astrocyte glycogen breaks down to lactate that is transferred to adjacent neural elements (both synapses in gray matter and axons in white matter) where it is used aerobically as fuel [27, 28, >>181<<, 252]. In addition, computer-based modeling studies suggest that during periods of high neuronal activity, inhibition of phosphofructokinase leads to impairment of neuronal glycolysis, with the consequence that lactate effluxed from" ; ns1:mentions . _:b6628434 rdf:type ns1:Context ; rdf:value "indicate that during hypoglycemia, astrocyte glycogen breaks down to lactate that is transferred to adjacent neural elements (both synapses in gray matter and axons in white matter) where it is used aerobically as fuel [27, 28, 181, >>252<<]. In addition, computer-based modeling studies suggest that during periods of high neuronal activity, inhibition of phosphofructokinase leads to impairment of neuronal glycolysis, with the consequence that lactate effluxed from astrocytes" ; ns1:mentions . _:b6628435 rdf:type ns1:Context ; rdf:value "that during periods of high neuronal activity, inhibition of phosphofructokinase leads to impairment of neuronal glycolysis, with the consequence that lactate effluxed from astrocytes becomes the preferred energy substrate for neurons [>>171<<]." ; ns1:mentions . _:b6628436 rdf:type ns1:Context ; rdf:value "The blood brain barrier (BBB) is a diffusion barrier that impedes the influx into brain parenchyma of certain molecules on the basis of polarity and size [>>1<<, 11]. The principal cellular constituents of the BBB are cerebral capillary endothelial cells that form tight junctions and are surrounded by a basal lamina, perivascular pericytes, and astrocyte endfeet." ; ns1:mentions . _:b6628437 rdf:type ns1:Context ; rdf:value "The blood brain barrier (BBB) is a diffusion barrier that impedes the influx into brain parenchyma of certain molecules on the basis of polarity and size [1, >>11<<]. The principal cellular constituents of the BBB are cerebral capillary endothelial cells that form tight junctions and are surrounded by a basal lamina, perivascular pericytes, and astrocyte endfeet." ; ns1:mentions . _:b6628438 rdf:type ns1:Context ; rdf:value "The main functional components of the BBB are the endothelial tight junctions [>>1<<, 11]. Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [1, 11," ; ns1:mentions . _:b6628439 rdf:type ns1:Context ; rdf:value "The main functional components of the BBB are the endothelial tight junctions [1, >>11<<]. Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [1, 11, 17," ; ns1:mentions . _:b6628440 rdf:type ns1:Context ; rdf:value "Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [>>1<<, 11, 17, 208]." ; ns1:mentions . _:b6628441 rdf:type ns1:Context ; rdf:value "Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [1, >>11<<, 17, 208]." ; ns1:mentions . _:b6628442 rdf:type ns1:Context ; rdf:value "Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [1, 11, >>17<<, 208]. In contrast, certain aspects of the BBB become functional in vivo before the appearance of astrocytes during development [93, 206]. In this regard, it is interesting to note that embryonic neural progenitor cells are able to induce" ; ns1:mentions . _:b6628443 rdf:type ns1:Context ; rdf:value "Numerous lines of in vitro evidence indicate that astrocytes can induce barrier properties in cerebral and other endothelial cells as well as in related epithelial, arguing in favor of a role for astrocytes in BBB induction [1, 11, 17, >>208<<]. In contrast, certain aspects of the BBB become functional in vivo before the appearance of astrocytes during development [93, 206]." ; ns1:mentions . _:b6628444 rdf:type ns1:Context ; rdf:value "In contrast, certain aspects of the BBB become functional in vivo before the appearance of astrocytes during development [>>93<<, 206]. In this regard, it is interesting to note that embryonic neural progenitor cells are able to induce BBB properties in cerebral endothelial cells [255]. Other studies suggest a role for astrocytes in regulating BBB properties of" ; ns1:mentions . _:b6628445 rdf:type ns1:Context ; rdf:value "In contrast, certain aspects of the BBB become functional in vivo before the appearance of astrocytes during development [93, >>206<<]. In this regard, it is interesting to note that embryonic neural progenitor cells are able to induce BBB properties in cerebral endothelial cells [255]. Other studies suggest a role for astrocytes in regulating BBB properties of cerebral" ; ns1:mentions . _:b6628446 rdf:type ns1:Context ; rdf:value "In this regard, it is interesting to note that embryonic neural progenitor cells are able to induce BBB properties in cerebral endothelial cells [>>255<<]. Other studies suggest a role for astrocytes in regulating BBB properties of cerebral endothelial in vivo in adult mice through specific BMP signaling mechanisms on astrocyte endfeet that when disrupted cause BBB leaks [6]. In addition," ; ns1:mentions . _:b6628447 rdf:type ns1:Context ; rdf:value "Other studies suggest a role for astrocytes in regulating BBB properties of cerebral endothelial in vivo in adult mice through specific BMP signaling mechanisms on astrocyte endfeet that when disrupted cause BBB leaks [>>6<<]. In addition, both astrocytes and related enteric glial cells are able to induce barrier properties in gut epithelial cells and the molecule GSNO has been identified as a molecular mediator of this effect [208]. Additional studies will" ; ns1:mentions . _:b6628448 rdf:type ns1:Context ; rdf:value "In addition, both astrocytes and related enteric glial cells are able to induce barrier properties in gut epithelial cells and the molecule GSNO has been identified as a molecular mediator of this effect [>>208<<]. Additional studies will be needed to clarify the roles of astrocytes and pericytes in BBB function and to identify molecular mediators that may induce BBB properties in cerebral endothelia. It is possible that different cell types" ; ns1:mentions . _:b6628449 rdf:type ns1:Context ; rdf:value "The increasing awareness of the complexity, importance, and diversity of astrocyte functions is giving rise to a growing interest in the potential for specialization and heterogeneity among astrocytes [>>96<<]. The notion of astrocyte heterogeneity is not new." ; ns1:mentions . _:b6628450 rdf:type ns1:Context ; rdf:value "astrocytes, various lines of evidence suggest that there is considerable molecular, structural, and potentially functional diversity of astrocytes at both the regional and local levels, but such investigations are at an early stage [>>10<<, 96]. In this context it is interesting to note that the number, complexity, and diversity of astroglial cells associated with neurons has increased considerably with evolution, such that the ratio of astrocytes to neurons is 1:" ; ns1:mentions . _:b6628451 rdf:type ns1:Context ; rdf:value "astrocytes, various lines of evidence suggest that there is considerable molecular, structural, and potentially functional diversity of astrocytes at both the regional and local levels, but such investigations are at an early stage [10, >>96<<]. In this context it is interesting to note that the number, complexity, and diversity of astroglial cells associated with neurons has increased considerably with evolution, such that the ratio of astrocytes to neurons is 1:" ; ns1:mentions . _:b6628452 rdf:type ns1:Context ; rdf:value "considerably with evolution, such that the ratio of astrocytes to neurons is 1:6 in worms, 1:3 in rodent cortex, and 1.4:1 in human cortex, implying that astrocyte roles increase in importance with sophistication of neural tissue [>>162<<]. The human cerebral neocortex contains multiple subtypes of astrocytes, including types that do not appear to exist in rodent cortex [170]." ; ns1:mentions . _:b6628453 rdf:type ns1:Context ; rdf:value "The human cerebral neocortex contains multiple subtypes of astrocytes, including types that do not appear to exist in rodent cortex [>>170<<]. As molecular markers become more sophisticated, it seems likely that astrocytes will be revealed to be considerably more heterogeneous than thus far imagined. Such information is likely to impact on concepts about astrocyte roles in" ; ns1:mentions . _:b6628454 rdf:type ns1:Context ; rdf:value "In the embryonic brain, it is now clear that radial cells are NSC that give rise to cortical pyramidal neurons [>>116<<, 134, 164]." ; ns1:mentions . _:b6628455 rdf:type ns1:Context ; rdf:value "In the embryonic brain, it is now clear that radial cells are NSC that give rise to cortical pyramidal neurons [116, >>134<<, 164]. As these radial cells mature, they adopt GFAP expression and some give rise to GFAP-expressing radial NSC that persist in juvenile and adult forebrain, while others become astrocytes [116, 122, 142]. Some GFAP-expressing radial NSC" ; ns1:mentions . _:b6628456 rdf:type ns1:Context ; rdf:value "In the embryonic brain, it is now clear that radial cells are NSC that give rise to cortical pyramidal neurons [116, 134, >>164<<]. As these radial cells mature, they adopt GFAP expression and some give rise to GFAP-expressing radial NSC that persist in juvenile and adult forebrain, while others become astrocytes [116, 122, 142]. Some GFAP-expressing radial NSC" ; ns1:mentions . _:b6628457 rdf:type ns1:Context ; rdf:value "As these radial cells mature, they adopt GFAP expression and some give rise to GFAP-expressing radial NSC that persist in juvenile and adult forebrain, while others become astrocytes [>>116<<, 122, 142]." ; ns1:mentions . _:b6628458 rdf:type ns1:Context ; rdf:value "As these radial cells mature, they adopt GFAP expression and some give rise to GFAP-expressing radial NSC that persist in juvenile and adult forebrain, while others become astrocytes [116, >>122<<, 142]. Some GFAP-expressing radial NSC remain constitutively active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the" ; ns1:mentions . _:b6628459 rdf:type ns1:Context ; rdf:value "As these radial cells mature, they adopt GFAP expression and some give rise to GFAP-expressing radial NSC that persist in juvenile and adult forebrain, while others become astrocytes [116, 122, >>142<<]. Some GFAP-expressing radial NSC remain constitutively active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the" ; ns1:mentions . _:b6628460 rdf:type ns1:Context ; rdf:value "constitutively active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the predominant source of adult neurogenesis [>>56<<, 78, 103, 214]." ; ns1:mentions . _:b6628461 rdf:type ns1:Context ; rdf:value "constitutively active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the predominant source of adult neurogenesis [56, >>78<<, 103, 214]." ; ns1:mentions . _:b6628462 rdf:type ns1:Context ; rdf:value "active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the predominant source of adult neurogenesis [56, 78, >>103<<, 214]. Based almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, 116], but it is not clear that such a nomenclature is either warranted or" ; ns1:mentions . _:b6628463 rdf:type ns1:Context ; rdf:value "active throughout life in the subependymal (or subventricular) zone of the lateral ventricles and in the subgranular zone of the hippocampal dentate gyrus, where they are the predominant source of adult neurogenesis [56, 78, 103, >>214<<]. Based almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, 116], but it is not clear that such a nomenclature is either warranted or useful" ; ns1:mentions . _:b6628464 rdf:type ns1:Context ; rdf:value "Based almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [>>56<<, 116], but it is not clear that such a nomenclature is either warranted or useful [14, 84, 153]." ; ns1:mentions . _:b6628465 rdf:type ns1:Context ; rdf:value "Based almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, >>116<<], but it is not clear that such a nomenclature is either warranted or useful [14, 84, 153]." ; ns1:mentions . _:b6628466 rdf:type ns1:Context ; rdf:value "Based almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, 116], but it is not clear that such a nomenclature is either warranted or useful [>>14<<, 84, 153]. There is ample evidence that GFAP is not an exclusive marker of astrocytes." ; ns1:mentions . _:b6628467 rdf:type ns1:Context ; rdf:value "almost entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, 116], but it is not clear that such a nomenclature is either warranted or useful [14, >>84<<, 153]. There is ample evidence that GFAP is not an exclusive marker of astrocytes." ; ns1:mentions . _:b6628468 rdf:type ns1:Context ; rdf:value "entirely on the observation that these adult NSC express GFAP, they have been referred to by some authors as a \u2018sub-type\u2019 of astrocyte [56, 116], but it is not clear that such a nomenclature is either warranted or useful [14, 84, >>153<<]. There is ample evidence that GFAP is not an exclusive marker of astrocytes." ; ns1:mentions . _:b6628469 rdf:type ns1:Context ; rdf:value "Differentiated astrocytes in uninjured mature cerebral cortex do not exhibit neurogenic potential either in vivo or in vitro [>>104<<]. Even proliferating reactive astrocytes after CNS trauma give rise only to other astrocytes and do not spontaneously exhibit multipotent neurogenic potential unless they are reprogrammed genetically or by exposure to high doses of" ; ns1:mentions . _:b6628470 rdf:type ns1:Context ; rdf:value "astrocytes after CNS trauma give rise only to other astrocytes and do not spontaneously exhibit multipotent neurogenic potential unless they are reprogrammed genetically or by exposure to high doses of specific growth factors in vitro [>>29<<, 30]. In addition, GFAP-expressing NSC differ in morphology (radial phenotype), chemical phenotype (LeX and nestin expression), and physiological characteristics from protoplasmic and fibrous astrocytes [78, 104, 126]." ; ns1:mentions . _:b6628471 rdf:type ns1:Context ; rdf:value "after CNS trauma give rise only to other astrocytes and do not spontaneously exhibit multipotent neurogenic potential unless they are reprogrammed genetically or by exposure to high doses of specific growth factors in vitro [29, >>30<<]. In addition, GFAP-expressing NSC differ in morphology (radial phenotype), chemical phenotype (LeX and nestin expression), and physiological characteristics from protoplasmic and fibrous astrocytes [78, 104, 126]." ; ns1:mentions . _:b6628472 rdf:type ns1:Context ; rdf:value "In addition, GFAP-expressing NSC differ in morphology (radial phenotype), chemical phenotype (LeX and nestin expression), and physiological characteristics from protoplasmic and fibrous astrocytes [>>78<<, 104, 126]." ; ns1:mentions . _:b6628473 rdf:type ns1:Context ; rdf:value "In addition, GFAP-expressing NSC differ in morphology (radial phenotype), chemical phenotype (LeX and nestin expression), and physiological characteristics from protoplasmic and fibrous astrocytes [78, >>104<<, 126]. Thus, the majority of currently available evidence argues that juvenile and adult NSC share more similarities with embryonic radial NSC than with mature astrocytes. There seems to be no reason to label the multipotent neural" ; ns1:mentions . _:b6628474 rdf:type ns1:Context ; rdf:value "In addition, GFAP-expressing NSC differ in morphology (radial phenotype), chemical phenotype (LeX and nestin expression), and physiological characteristics from protoplasmic and fibrous astrocytes [78, 104, >>126<<]. Thus, the majority of currently available evidence argues that juvenile and adult NSC share more similarities with embryonic radial NSC than with mature astrocytes. There seems to be no reason to label the multipotent neural progenitors" ; ns1:mentions . _:b6628475 rdf:type ns1:Context ; rdf:value "It has been argued that it may be useful to return to the nomenclature of early neuroanatomists who referred to such radial progenitor cells as \u2018neuroepithelial cells\u2019 rather than glia [>>14<<, 153]. Regardless of nomenclature, the presence in certain forebrain areas of GFAP-expressing cells that have constitutive multipotent NSC potential throughout life has important implications for concepts regarding various CNS disorders," ; ns1:mentions . _:b6628476 rdf:type ns1:Context ; rdf:value "It has been argued that it may be useful to return to the nomenclature of early neuroanatomists who referred to such radial progenitor cells as \u2018neuroepithelial cells\u2019 rather than glia [14, >>153<<]. Regardless of nomenclature, the presence in certain forebrain areas of GFAP-expressing cells that have constitutive multipotent NSC potential throughout life has important implications for concepts regarding various CNS disorders, in" ; ns1:mentions . _:b6628477 rdf:type ns1:Context ; rdf:value "Enteric glia surround neuronal cell bodies and axons, as well as contact blood vessels and epithelial cells, and are likely to take part in many gut functions in manners that are similar to astrocytes [>>32<<, 202]. GFAP is expressed widely in many tissues by a variety of cell types including mesenchymal stellate cells that share structural and functional similarities with astrocytes in many organs, including liver, kidney, pancreas, lungs," ; ns1:mentions . _:b6628478 rdf:type ns1:Context ; rdf:value "Enteric glia surround neuronal cell bodies and axons, as well as contact blood vessels and epithelial cells, and are likely to take part in many gut functions in manners that are similar to astrocytes [32, >>202<<]. GFAP is expressed widely in many tissues by a variety of cell types including mesenchymal stellate cells that share structural and functional similarities with astrocytes in many organs, including liver, kidney, pancreas, lungs, and" ; ns1:mentions . _:b6628479 rdf:type ns1:Context ; rdf:value "is expressed widely in many tissues by a variety of cell types including mesenchymal stellate cells that share structural and functional similarities with astrocytes in many organs, including liver, kidney, pancreas, lungs, and testes [>>32<<, 124, 266]." ; ns1:mentions . _:b6628480 rdf:type ns1:Context ; rdf:value "widely in many tissues by a variety of cell types including mesenchymal stellate cells that share structural and functional similarities with astrocytes in many organs, including liver, kidney, pancreas, lungs, and testes [32, >>124<<, 266]. The functional roles of these cells and their potential similarities with astrocytes are only beginning to be explored, but some appear to share with astrocytes functions in tissue repair and scar formation, as well as newly" ; ns1:mentions . _:b6628481 rdf:type ns1:Context ; rdf:value "widely in many tissues by a variety of cell types including mesenchymal stellate cells that share structural and functional similarities with astrocytes in many organs, including liver, kidney, pancreas, lungs, and testes [32, 124, >>266<<]. The functional roles of these cells and their potential similarities with astrocytes are only beginning to be explored, but some appear to share with astrocytes functions in tissue repair and scar formation, as well as newly discovered" ; ns1:mentions . _:b6628482 rdf:type ns4:Section ; dc:title "reactive astrogliosis and glial scar formation" ; ns4:contains _:b6628576 , _:b6628577 , _:b6628578 , _:b6628556 , _:b6628557 , _:b6628558 , _:b6628559 , _:b6628552 , _:b6628553 , _:b6628554 , _:b6628555 , _:b6628548 , _:b6628549 , _:b6628550 , _:b6628551 , _:b6628544 , _:b6628545 , _:b6628546 , _:b6628547 , _:b6628572 , _:b6628573 , _:b6628574 , _:b6628575 , _:b6628568 , _:b6628569 , _:b6628570 , _:b6628571 , _:b6628564 , _:b6628565 , _:b6628566 , _:b6628567 , _:b6628560 , _:b6628561 , _:b6628562 , _:b6628563 , _:b6628524 , _:b6628525 , _:b6628526 , _:b6628527 , _:b6628520 , _:b6628521 , _:b6628522 , _:b6628523 , _:b6628516 , _:b6628517 , _:b6628518 , _:b6628519 , _:b6628512 , _:b6628513 , _:b6628514 , _:b6628515 , _:b6628540 , _:b6628541 , _:b6628542 , _:b6628543 , _:b6628536 , _:b6628537 , _:b6628538 , _:b6628539 , _:b6628532 , _:b6628533 , _:b6628534 , _:b6628535 , _:b6628528 , _:b6628529 , _:b6628530 , _:b6628531 , _:b6628492 , _:b6628493 , _:b6628494 , _:b6628495 , _:b6628488 , _:b6628489 , _:b6628490 , _:b6628491 , _:b6628484 , _:b6628485 , _:b6628486 , _:b6628487 , _:b6628483 , _:b6628508 , _:b6628509 , _:b6628510 , _:b6628511 , _:b6628504 , _:b6628505 , _:b6628506 , _:b6628507 , _:b6628500 , _:b6628501 , _:b6628502 , _:b6628503 , _:b6628496 , _:b6628497 , _:b6628498 , _:b6628499 . _:b6628483 rdf:type ns1:Context ; rdf:value "Based on a large body of observations in experimental animals, a definition of reactive astrogliosis has recently been proposed [>>226<<] that encompasses four key features:" ; ns1:mentions . _:b6628484 rdf:type ns1:Context ; rdf:value "the changes undergone during reactive astrogliosis have the potential to alter astrocyte activities both through gain and loss of functions that can impact both beneficially and detrimentally on surrounding neural and non-neural cells [>>226<<]. Here, we propose to apply and extend this definition to identifying different gradations of reactive astrogliosis and glial scar formation that may be encountered in histopathological examinations of human disorders (Figs." ; ns1:mentions . _:b6628485 rdf:type ns1:Context ; rdf:value "In mild or moderate reactive astrogliosis there is variable up regulation of expression of GFAP and other genes [>>226<<], as well as hypertrophy of cell body and processes that can vary in degree but that occurs within the domains of individual astrocytes [257] without substantive intermingling or overlap of processes of neighboring astrocytes or loss of" ; ns1:mentions . _:b6628486 rdf:type ns1:Context ; rdf:value "reactive astrogliosis there is variable up regulation of expression of GFAP and other genes [226], as well as hypertrophy of cell body and processes that can vary in degree but that occurs within the domains of individual astrocytes [>>257<<] without substantive intermingling or overlap of processes of neighboring astrocytes or loss of individual domains (Figs." ; ns1:mentions . _:b6628487 rdf:type ns1:Context ; rdf:value "3b, 4b) [>>226<<]. There is little or no astrocyte proliferation in mild or moderate reactive astrogliosis; however, the up regulation of GFAP expression in astrocytes that do not express detectable levels of GFAP in healthy tissue (Figs." ; ns1:mentions . _:b6628488 rdf:type ns1:Context ; rdf:value "tissue architecture, if the triggering mechanism is able to resolve, then mild or moderate reactive astrogliosis exhibits the potential for resolution in which the astrocytes return to an appearance similar to that in healthy tissue [>>226<<]. The physiological consequences of mild or moderate reactive astrogliosis are not well understood." ; ns1:mentions . _:b6628489 rdf:type ns1:Context ; rdf:value "scars act as neuroprotective barriers to inflammatory cells and infectious agents, and that they form in particular along borders to severe tissue damage, necrosis, infection or autoimmune-triggered inflammatory infiltration (Fig.\u00A04d) [>>33<<, 59, 68, 95, 226, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628490 rdf:type ns1:Context ; rdf:value "4d) [33, >>59<<, 68, 95, 226, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628491 rdf:type ns1:Context ; rdf:value "4d) [33, 59, >>68<<, 95, 226, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628492 rdf:type ns1:Context ; rdf:value "4d) [33, 59, 68, >>95<<, 226, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628493 rdf:type ns1:Context ; rdf:value "4d) [33, 59, 68, 95, >>226<<, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628494 rdf:type ns1:Context ; rdf:value "4d) [33, 59, 68, 95, 226, >>251<<]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig." ; ns1:mentions . _:b6628495 rdf:type ns1:Context ; rdf:value "inflammatory infiltration (Fig.\u00A04d) [33, 59, 68, 95, 226, 251]. An important feature of these glial scars is the interaction of reactive astrocytes with other cell types, in particular fibromeningeal and other glial cells (Fig.\u00A04d) [>>31<<, 95], and the deposition of a dense collagenous extracellular matrix that contains many molecular cues that inhibit axonal and cellular migration [219]." ; ns1:mentions . _:b6628496 rdf:type ns1:Context ; rdf:value "4d) [31, >>95<<], and the deposition of a dense collagenous extracellular matrix that contains many molecular cues that inhibit axonal and cellular migration [219]." ; ns1:mentions . _:b6628497 rdf:type ns1:Context ; rdf:value "4d) [31, 95], and the deposition of a dense collagenous extracellular matrix that contains many molecular cues that inhibit axonal and cellular migration [>>219<<]. Triggering insults include penetrating trauma, severe contusive trauma, invasive infections or abscess formation, neoplasm, chronic neurodegeneration, systemically triggered inflammatory challenges. It is noteworthy that the glial scar" ; ns1:mentions . _:b6628498 rdf:type ns1:Context ; rdf:value "In healthy CNS tissue, astrocyte turnover is low and there are few proliferating or newly generated astrocytes and it appears that the majority of astrocytes are post-mitotic and long-lived [>>33<<, 45, 97, 167]." ; ns1:mentions . _:b6628499 rdf:type ns1:Context ; rdf:value "In healthy CNS tissue, astrocyte turnover is low and there are few proliferating or newly generated astrocytes and it appears that the majority of astrocytes are post-mitotic and long-lived [33, >>45<<, 97, 167]." ; ns1:mentions . _:b6628500 rdf:type ns1:Context ; rdf:value "In healthy CNS tissue, astrocyte turnover is low and there are few proliferating or newly generated astrocytes and it appears that the majority of astrocytes are post-mitotic and long-lived [33, 45, >>97<<, 167]. Experimental analysis of cell proliferation indicates that GFAP up regulation and hypertrophy can occur in mild or moderate astrogliosis in the absence of proliferation and increase in cell number [226]. The appearance of newly" ; ns1:mentions . _:b6628501 rdf:type ns1:Context ; rdf:value "In healthy CNS tissue, astrocyte turnover is low and there are few proliferating or newly generated astrocytes and it appears that the majority of astrocytes are post-mitotic and long-lived [33, 45, 97, >>167<<]. Experimental analysis of cell proliferation indicates that GFAP up regulation and hypertrophy can occur in mild or moderate astrogliosis in the absence of proliferation and increase in cell number [226]. The appearance of newly" ; ns1:mentions . _:b6628502 rdf:type ns1:Context ; rdf:value "Experimental analysis of cell proliferation indicates that GFAP up regulation and hypertrophy can occur in mild or moderate astrogliosis in the absence of proliferation and increase in cell number [>>226<<]. The appearance of newly proliferated astrocytes occurs in severe diffuse reactive astrogliosis and severe reactive astrogliosis with compact glial scar formation as discussed above (Figs.\u00A03c, 4c, d). In human specimens, actively" ; ns1:mentions . _:b6628503 rdf:type ns1:Context ; rdf:value "In human specimens, actively dividing reactive astrocytes have been particularly reported in association with infection and acute demyelinating lesions [>>45<<]. The source of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33," ; ns1:mentions . _:b6628504 rdf:type ns1:Context ; rdf:value "The source of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [>>30<<, 33, 37, 77, 133, 141, 226]." ; ns1:mentions . _:b6628505 rdf:type ns1:Context ; rdf:value "The source of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, >>33<<, 37, 77, 133, 141, 226]." ; ns1:mentions . _:b6628506 rdf:type ns1:Context ; rdf:value "The source of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33, >>37<<, 77, 133, 141, 226]." ; ns1:mentions . _:b6628507 rdf:type ns1:Context ; rdf:value "source of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33, 37, >>77<<, 133, 141, 226]." ; ns1:mentions . _:b6628508 rdf:type ns1:Context ; rdf:value "of newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33, 37, 77, >>133<<, 141, 226]." ; ns1:mentions . _:b6628509 rdf:type ns1:Context ; rdf:value "newly divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33, 37, 77, 133, >>141<<, 226]." ; ns1:mentions . _:b6628510 rdf:type ns1:Context ; rdf:value "divided scar-forming astrocytes is not well established, and may include mature astrocytes that re-enter the cell cycle as well as progenitor cells in the local parenchyma or in the periventricular regions [30, 33, 37, 77, 133, 141, >>226<<]." ; ns1:mentions . _:b6628511 rdf:type ns1:Context ; rdf:value "(7) products associated with neurodegeneration such as \u03B2-amyloid, (8) molecules associated with systemic metabolic toxicity such as NH4 +, and (9) regulators of cell proliferation such endothelin-1, as reviewed in detail elsewhere [>>226<<]. Such molecular mediators of reactive astrogliosis can be released by all cell types in CNS tissue, including neurons, microglia, oligodendrocyte lineage cells, pericytes, endothelia, and other astrocytes, in response to all forms of CNS" ; ns1:mentions . _:b6628512 rdf:type ns1:Context ; rdf:value "stretching as might be encountered during acceleration/deceleration CNS injury and which releases ATP, to intense tissue injury and cell death that release various intracellular molecules that signal intense tissue damage (Fig.\u00A02b) [>>226<<]. It is also becoming clear that different molecular, morphological, and functional changes in reactive astrocytes are specifically controlled by inter- and intra-cellular signaling mechanisms that reflect the specific contexts of the" ; ns1:mentions . _:b6628513 rdf:type ns1:Context ; rdf:value "changes in reactive astrocytes are specifically controlled by inter- and intra-cellular signaling mechanisms that reflect the specific contexts of the stimuli and produce specific and gradated responses of reactive astrogliosis [>>226<<]. For example, the different intracellular signaling pathways associated with STAT3, NF\u03BAB, SOCS3, Nrf2, cAMP, Olig2 are implicated in mediating different aspects or different degrees of reactive astrogliosis such as GFAP up regulation," ; ns1:mentions . _:b6628514 rdf:type ns1:Context ; rdf:value "with STAT3, NF\u03BAB, SOCS3, Nrf2, cAMP, Olig2 are implicated in mediating different aspects or different degrees of reactive astrogliosis such as GFAP up regulation, cell hypertrophy, proliferation, and pro- or anti-inflammatory effects [>>226<<]. Molecular triggers that lead to proliferation of reactive astrocytes in vivo are incompletely characterized but include EGF, FGF, endothelin 1, and ATP [77, 121, 161]." ; ns1:mentions . _:b6628515 rdf:type ns1:Context ; rdf:value "Molecular triggers that lead to proliferation of reactive astrocytes in vivo are incompletely characterized but include EGF, FGF, endothelin 1, and ATP [>>77<<, 121, 161]." ; ns1:mentions . _:b6628516 rdf:type ns1:Context ; rdf:value "Molecular triggers that lead to proliferation of reactive astrocytes in vivo are incompletely characterized but include EGF, FGF, endothelin 1, and ATP [77, >>121<<, 161]." ; ns1:mentions . _:b6628517 rdf:type ns1:Context ; rdf:value "Molecular triggers that lead to proliferation of reactive astrocytes in vivo are incompletely characterized but include EGF, FGF, endothelin 1, and ATP [77, 121, >>161<<]." ; ns1:mentions . _:b6628518 rdf:type ns1:Context ; rdf:value "As reviewed in detail elsewhere [>>226<<], many studies using transgenic and experimental animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from" ; ns1:mentions . _:b6628519 rdf:type ns1:Context ; rdf:value "As reviewed in detail elsewhere [226], many studies using transgenic and experimental animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [>>33<<, 198, 234], (2) protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta" ; ns1:mentions . _:b6628520 rdf:type ns1:Context ; rdf:value "reviewed in detail elsewhere [226], many studies using transgenic and experimental animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, >>198<<, 234], (2) protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta" ; ns1:mentions . _:b6628521 rdf:type ns1:Context ; rdf:value "in detail elsewhere [226], many studies using transgenic and experimental animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, >>234<<], (2) protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides" ; ns1:mentions . _:b6628522 rdf:type ns1:Context ; rdf:value "animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [>>42<<, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing" ; ns1:mentions . _:b6628523 rdf:type ns1:Context ; rdf:value "animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [42, >>216<<, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing" ; ns1:mentions . _:b6628524 rdf:type ns1:Context ; rdf:value "models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [42, 216, >>234<<, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic" ; ns1:mentions . _:b6628525 rdf:type ns1:Context ; rdf:value "models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [42, 216, 234, >>245<<], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema" ; ns1:mentions . _:b6628526 rdf:type ns1:Context ; rdf:value "astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [>>125<<], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive" ; ns1:mentions . _:b6628527 rdf:type ns1:Context ; rdf:value "(1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [>>193<<], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [33, 264], (8) stabilizing extracellular" ; ns1:mentions . _:b6628528 rdf:type ns1:Context ; rdf:value "protection from oxidative stress via glutathione production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [>>113<<], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [33, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and" ; ns1:mentions . _:b6628529 rdf:type ns1:Context ; rdf:value "production [42, 216, 234, 245], (3) neuroprotection via adenosine release [125], (4) protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [>>33<<], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [33, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or" ; ns1:mentions . _:b6628530 rdf:type ns1:Context ; rdf:value "protection from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [>>33<<, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59," ; ns1:mentions . _:b6628531 rdf:type ns1:Context ; rdf:value "from NH4 + toxicity [193], (5) neuroprotection by degradation of amyloid-beta peptides [113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [33, >>264<<], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68," ; ns1:mentions . _:b6628532 rdf:type ns1:Context ; rdf:value "[113], (6) facilitating blood brain barrier repair [33], (7) reducing vasogenic edema after trauma, stroke or obstructive hydrocephalus [33, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [>>264<<], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, 95, 123, 156, 175, 251]." ; ns1:mentions . _:b6628533 rdf:type ns1:Context ; rdf:value "[33, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [>>33<<, 59, 68, 95, 123, 156, 175, 251]." ; ns1:mentions . _:b6628534 rdf:type ns1:Context ; rdf:value "[33, 264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, >>59<<, 68, 95, 123, 156, 175, 251]." ; ns1:mentions . _:b6628535 rdf:type ns1:Context ; rdf:value "264], (8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, >>68<<, 95, 123, 156, 175, 251]." ; ns1:mentions . _:b6628536 rdf:type ns1:Context ; rdf:value "(8) stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, >>95<<, 123, 156, 175, 251]." ; ns1:mentions . _:b6628537 rdf:type ns1:Context ; rdf:value "stabilizing extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, 95, >>123<<, 156, 175, 251]." ; ns1:mentions . _:b6628538 rdf:type ns1:Context ; rdf:value "extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, 95, 123, >>156<<, 175, 251]." ; ns1:mentions . _:b6628539 rdf:type ns1:Context ; rdf:value "extracellular fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, 95, 123, 156, >>175<<, 251]." ; ns1:mentions . _:b6628540 rdf:type ns1:Context ; rdf:value "fluid and ion balance and reducing seizure threshold [264], and (9) limiting the spread of inflammatory cells or infectious agents from areas of damage or disease into healthy CNS parenchyma [33, 59, 68, 95, 123, 156, 175, >>251<<]." ; ns1:mentions . _:b6628541 rdf:type ns1:Context ; rdf:value "Of particular interest as regards functions of reactive astrocytes, is recent evidence that reactive astrogliosis and glial scar formation play essential roles in regulating CNS inflammation [>>226<<]. In response to different kinds of stimulation, reactive astrocytes can make many different kinds of molecules with either pro- or anti-inflammatory potential [60, 108] and reactive astrocytes can exert both pro- and anti-inflammatory" ; ns1:mentions . _:b6628542 rdf:type ns1:Context ; rdf:value "In response to different kinds of stimulation, reactive astrocytes can make many different kinds of molecules with either pro- or anti-inflammatory potential [>>60<<, 108] and reactive astrocytes can exert both pro- and anti-inflammatory effects on microglia [67, 148]." ; ns1:mentions . _:b6628543 rdf:type ns1:Context ; rdf:value "In response to different kinds of stimulation, reactive astrocytes can make many different kinds of molecules with either pro- or anti-inflammatory potential [60, >>108<<] and reactive astrocytes can exert both pro- and anti-inflammatory effects on microglia [67, 148]." ; ns1:mentions . _:b6628544 rdf:type ns1:Context ; rdf:value "kinds of stimulation, reactive astrocytes can make many different kinds of molecules with either pro- or anti-inflammatory potential [60, 108] and reactive astrocytes can exert both pro- and anti-inflammatory effects on microglia [>>67<<, 148]. A large body of experimental studies indicates that reactive astrocytes can exert both pro- and anti-inflammatory regulatory functions in vivo in a context dependent manner that is regulated by specific molecular signaling pathways" ; ns1:mentions . _:b6628545 rdf:type ns1:Context ; rdf:value "kinds of stimulation, reactive astrocytes can make many different kinds of molecules with either pro- or anti-inflammatory potential [60, 108] and reactive astrocytes can exert both pro- and anti-inflammatory effects on microglia [67, >>148<<]. A large body of experimental studies indicates that reactive astrocytes can exert both pro- and anti-inflammatory regulatory functions in vivo in a context dependent manner that is regulated by specific molecular signaling pathways" ; ns1:mentions . _:b6628546 rdf:type ns1:Context ; rdf:value "A large body of experimental studies indicates that reactive astrocytes can exert both pro- and anti-inflammatory regulatory functions in vivo in a context dependent manner that is regulated by specific molecular signaling pathways [>>226<<]. A functional model, which may reconcile the apparent paradox that reactive astrocytes have the potential to exert both pro- and anti-inflammatory activities, is that reactive astrocytes exert different activities at different times" ; ns1:mentions . _:b6628547 rdf:type ns1:Context ; rdf:value "4d) [225, >>226<<]. Together, these findings indicate that there is a normal process of reactive astrogliosis and glial scar formation that exerts various beneficial functions including protecting neural cells and function, restricting the spread of" ; ns1:mentions . _:b6628548 rdf:type ns1:Context ; rdf:value "of the process of reactive astrogliosis and scar formation have the potential to contribute to, or to be primary causes of, CNS disease mechanisms either through loss of normal functions or through gain of detrimental effects [>>226<<]." ; ns1:mentions . _:b6628549 rdf:type ns1:Context ; rdf:value "for ways in which loss or attenuation of reactive astrocyte functions might worsen outcome after various kinds of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [>>33<<, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, 68, 95, 251]." ; ns1:mentions . _:b6628550 rdf:type ns1:Context ; rdf:value "for ways in which loss or attenuation of reactive astrocyte functions might worsen outcome after various kinds of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, >>198<<, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, 68, 95, 251]." ; ns1:mentions . _:b6628551 rdf:type ns1:Context ; rdf:value "ways in which loss or attenuation of reactive astrocyte functions might worsen outcome after various kinds of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, >>234<<] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, 68, 95, 251]." ; ns1:mentions . _:b6628552 rdf:type ns1:Context ; rdf:value "kinds of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [>>33<<, 59, 68, 95, 251]. Clinical studies, discussed below, are also identifying a rapidly growing number of conditions that are precipitated by or exacerbated loss of functions by astrocytes or reactive astrocytes." ; ns1:mentions . _:b6628553 rdf:type ns1:Context ; rdf:value "kinds of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, >>59<<, 68, 95, 251]. Clinical studies, discussed below, are also identifying a rapidly growing number of conditions that are precipitated by or exacerbated loss of functions by astrocytes or reactive astrocytes." ; ns1:mentions . _:b6628554 rdf:type ns1:Context ; rdf:value "of CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, >>68<<, 95, 251]. Clinical studies, discussed below, are also identifying a rapidly growing number of conditions that are precipitated by or exacerbated loss of functions by astrocytes or reactive astrocytes." ; ns1:mentions . _:b6628555 rdf:type ns1:Context ; rdf:value "CNS insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, 68, >>95<<, 251]. Clinical studies, discussed below, are also identifying a rapidly growing number of conditions that are precipitated by or exacerbated loss of functions by astrocytes or reactive astrocytes." ; ns1:mentions . _:b6628556 rdf:type ns1:Context ; rdf:value "insults, for example, through excitotoxic neurodegeneration due to failure or attenuation of glutamate uptake [33, 198, 234] or increased inflammation or infection due to loss or failure of astrocyte barrier functions [33, 59, 68, 95, >>251<<]. Clinical studies, discussed below, are also identifying a rapidly growing number of conditions that are precipitated by or exacerbated loss of functions by astrocytes or reactive astrocytes." ; ns1:mentions . _:b6628557 rdf:type ns1:Context ; rdf:value "gain of a detrimental effect by reactive astrogliosis and glial scar formation is the inhibition of axon regeneration, first proposed over 100\u00A0years ago and now supported by extensive molecular and cell-biological evidence [>>219<<]. In addition, there is also evidence from both clinical (discussed below) and experimental studies that, under specific circumstances, astrocytes or reactive astrocytes have the potential to exert a variety of other detrimental effects" ; ns1:mentions . _:b6628558 rdf:type ns1:Context ; rdf:value "2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [>>22<<, 23], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due" ; ns1:mentions . _:b6628559 rdf:type ns1:Context ; rdf:value "2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [22, >>23<<], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to" ; ns1:mentions . _:b6628560 rdf:type ns1:Context ; rdf:value "2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [>>92<<, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma" ; ns1:mentions . _:b6628561 rdf:type ns1:Context ; rdf:value "2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [92, >>234<<], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and" ; ns1:mentions . _:b6628562 rdf:type ns1:Context ; rdf:value "2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [>>238<<], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [264], and (7)" ; ns1:mentions . _:b6628563 rdf:type ns1:Context ; rdf:value "(1) exacerbating inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [>>106<<, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [264], and (7) contributing to chronic pain [147]." ; ns1:mentions . _:b6628564 rdf:type ns1:Context ; rdf:value "inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, >>240<<], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [264], and (7) contributing to chronic pain [147]." ; ns1:mentions . _:b6628565 rdf:type ns1:Context ; rdf:value "levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [>>7<<], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [264], and (7) contributing to chronic pain [147]." ; ns1:mentions . _:b6628566 rdf:type ns1:Context ; rdf:value "glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [>>264<<], and (7) contributing to chronic pain [147]." ; ns1:mentions . _:b6628567 rdf:type ns1:Context ; rdf:value "to seizure genesis [106, 240], (5) compromising blood brain barrier function due to VEGF-production [7], (6) causing cytotoxic edema during trauma and stroke through AQP4 over activity [264], and (7) contributing to chronic pain [>>147<<]. There also appears to be the potential for combinatorial signaling cascades resulting from exposure to microbial antigens such as lipopolysaccharide (LPS), to markedly increase the production of potentially toxic molecules by astrocytes" ; ns1:mentions . _:b6628568 rdf:type ns1:Context ; rdf:value "also appears to be the potential for combinatorial signaling cascades resulting from exposure to microbial antigens such as lipopolysaccharide (LPS), to markedly increase the production of potentially toxic molecules by astrocytes [>>67<<, 92]. Context-dependent acute or chronic combinatorial signaling events (Fig." ; ns1:mentions . _:b6628569 rdf:type ns1:Context ; rdf:value "also appears to be the potential for combinatorial signaling cascades resulting from exposure to microbial antigens such as lipopolysaccharide (LPS), to markedly increase the production of potentially toxic molecules by astrocytes [67, >>92<<]. Context-dependent acute or chronic combinatorial signaling events (Fig." ; ns1:mentions . _:b6628570 rdf:type ns1:Context ; rdf:value "and glial scar formation make use of transgenic technologies combined with experimental animal models, which has revolutionized the study of neural injury and disease by allowing in vivo dissection of molecular and cellular mechanisms [>>226<<]. Nevertheless, in interpreting results derived from studies using transgenic mice it is important to understand associated caveats [226]." ; ns1:mentions . _:b6628571 rdf:type ns1:Context ; rdf:value "Nevertheless, in interpreting results derived from studies using transgenic mice it is important to understand associated caveats [>>226<<]. For example, different promoters (human or mouse GFAP, GLAST, etc.) may have different targeting properties/efficiencies as regards astrocytes and related cells. Although not all astrocytes express GFAP or GFAP-regulated transgenes in" ; ns1:mentions . _:b6628572 rdf:type ns1:Context ; rdf:value "Although not all astrocytes express GFAP or GFAP-regulated transgenes in healthy tissue, most if not all appear to do so after CNS injury or other insults [>>33<<, 95, 251]." ; ns1:mentions . _:b6628573 rdf:type ns1:Context ; rdf:value "Although not all astrocytes express GFAP or GFAP-regulated transgenes in healthy tissue, most if not all appear to do so after CNS injury or other insults [33, >>95<<, 251]. It is essential that authors define transgene expression levels individually and specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from" ; ns1:mentions . _:b6628574 rdf:type ns1:Context ; rdf:value "Although not all astrocytes express GFAP or GFAP-regulated transgenes in healthy tissue, most if not all appear to do so after CNS injury or other insults [33, 95, >>251<<]. It is essential that authors define transgene expression levels individually and specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from" ; ns1:mentions . _:b6628575 rdf:type ns1:Context ; rdf:value "and specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from transgene expression in other cells both within and outside of the CNS [>>33<<, 95, 226, 251]." ; ns1:mentions . _:b6628576 rdf:type ns1:Context ; rdf:value "and specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from transgene expression in other cells both within and outside of the CNS [33, >>95<<, 226, 251]." ; ns1:mentions . _:b6628577 rdf:type ns1:Context ; rdf:value "and specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from transgene expression in other cells both within and outside of the CNS [33, 95, >>226<<, 251]." ; ns1:mentions . _:b6628578 rdf:type ns1:Context ; rdf:value "specifically in every tissue region and experimental model being studied, as well as control for any possible confounding effects that may result from transgene expression in other cells both within and outside of the CNS [33, 95, 226, >>251<<]." ; ns1:mentions . _:b6628579 rdf:type ns4:Section ; dc:title "astrocyte appearance and roles in cns disorders and pathology" ; ns4:contains _:b6628712 , _:b6628713 , _:b6628714 , _:b6628715 , _:b6628716 , _:b6628717 , _:b6628718 , _:b6628719 , _:b6628704 , _:b6628705 , _:b6628706 , _:b6628707 , _:b6628708 , _:b6628709 , _:b6628710 , _:b6628711 , _:b6628728 , _:b6628729 , _:b6628730 , _:b6628731 , _:b6628732 , _:b6628733 , _:b6628734 , _:b6628735 , _:b6628720 , _:b6628721 , _:b6628722 , _:b6628723 , _:b6628724 , _:b6628725 , _:b6628726 , _:b6628727 , _:b6628680 , _:b6628681 , _:b6628682 , _:b6628683 , _:b6628684 , _:b6628685 , _:b6628686 , _:b6628687 , _:b6628672 , _:b6628673 , _:b6628674 , _:b6628675 , _:b6628676 , _:b6628677 , _:b6628678 , _:b6628679 , _:b6628696 , _:b6628697 , _:b6628698 , _:b6628699 , _:b6628700 , _:b6628701 , _:b6628702 , _:b6628703 , _:b6628688 , _:b6628689 , _:b6628690 , _:b6628691 , _:b6628692 , _:b6628693 , _:b6628694 , _:b6628695 , _:b6628648 , _:b6628649 , _:b6628650 , _:b6628651 , _:b6628652 , _:b6628653 , _:b6628654 , _:b6628655 , _:b6628640 , _:b6628641 , _:b6628642 , _:b6628643 , _:b6628644 , _:b6628645 , _:b6628646 , _:b6628647 , _:b6628664 , _:b6628665 , _:b6628666 , _:b6628667 , _:b6628668 , _:b6628669 , _:b6628670 , _:b6628671 , _:b6628656 , _:b6628657 , _:b6628658 , _:b6628659 , _:b6628660 , _:b6628661 , _:b6628662 , _:b6628663 , _:b6628616 , _:b6628617 , _:b6628618 , _:b6628619 , _:b6628620 , _:b6628621 , _:b6628622 , _:b6628623 , _:b6628608 , _:b6628609 , _:b6628610 , _:b6628611 , _:b6628612 , _:b6628613 , _:b6628614 , _:b6628615 , _:b6628632 , _:b6628633 , _:b6628634 , _:b6628635 , _:b6628636 , _:b6628637 , _:b6628638 , _:b6628639 , _:b6628624 , _:b6628625 , _:b6628626 , _:b6628627 , _:b6628628 , _:b6628629 , _:b6628630 , _:b6628631 , _:b6628768 , _:b6628769 , _:b6628770 , _:b6628771 , _:b6628772 , _:b6628744 , _:b6628745 , _:b6628746 , _:b6628747 , _:b6628748 , _:b6628749 , _:b6628750 , _:b6628751 , _:b6628736 , _:b6628737 , _:b6628738 , _:b6628739 , _:b6628740 , _:b6628741 , _:b6628742 , _:b6628743 , _:b6628760 , _:b6628761 , _:b6628762 , _:b6628763 , _:b6628764 , _:b6628765 , _:b6628766 , _:b6628767 , _:b6628752 , _:b6628753 , _:b6628754 , _:b6628755 , _:b6628756 , _:b6628757 , _:b6628758 , _:b6628759 , _:b6628584 , _:b6628585 , _:b6628586 , _:b6628587 , _:b6628588 , _:b6628589 , _:b6628590 , _:b6628591 , _:b6628580 , _:b6628581 , _:b6628582 , _:b6628583 , _:b6628600 , _:b6628601 , _:b6628602 , _:b6628603 , _:b6628604 , _:b6628605 , _:b6628606 , _:b6628607 , _:b6628592 , _:b6628593 , _:b6628594 , _:b6628595 , _:b6628596 , _:b6628597 , _:b6628598 , _:b6628599 . _:b6628580 rdf:type ns1:Context ; rdf:value "Traumatic brain and spinal cord injury are major causes of premature death, permanent physical disability, or long-lasting neuropsychiatric impairment [>>138<<]. Reactive astrogliosis and glial scar formation are prominent features of CNS trauma and are increasingly implicated as playing important roles in determining long-term clinical outcome [41, 226]." ; ns1:mentions . _:b6628581 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis and glial scar formation are prominent features of CNS trauma and are increasingly implicated as playing important roles in determining long-term clinical outcome [>>41<<, 226]. The appearance of reactive astrogliosis after CNS trauma (whether in the brain or spinal cord) varies with the (1) type of the trauma, i.e., whether it is penetrating, contusional, or diffuse (as in the case of diffuse axonal" ; ns1:mentions . _:b6628582 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis and glial scar formation are prominent features of CNS trauma and are increasingly implicated as playing important roles in determining long-term clinical outcome [41, >>226<<]. The appearance of reactive astrogliosis after CNS trauma (whether in the brain or spinal cord) varies with the (1) type of the trauma, i.e., whether it is penetrating, contusional, or diffuse (as in the case of diffuse axonal injury)," ; ns1:mentions . _:b6628583 rdf:type ns1:Context ; rdf:value "Severe reactive astrogliosis and glial scar formation at sites of CNS trauma are well documented to inhibit axonal regeneration [>>219<<] and are widely regarded as detrimental to clinical outcome." ; ns1:mentions . _:b6628584 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [>>33<<, 68, 95, 144, 175, 226] as discussed earlier." ; ns1:mentions . _:b6628585 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [33, >>68<<, 95, 144, 175, 226] as discussed earlier." ; ns1:mentions . _:b6628586 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [33, 68, >>95<<, 144, 175, 226] as discussed earlier." ; ns1:mentions . _:b6628587 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [33, 68, 95, >>144<<, 175, 226] as discussed earlier." ; ns1:mentions . _:b6628588 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [33, 68, 95, 144, >>175<<, 226] as discussed earlier." ; ns1:mentions . _:b6628589 rdf:type ns1:Context ; rdf:value "Nevertheless, recent studies using transgenic mouse models indicate that scar-forming reactive astrocytes exert essential neuroprotective functions after both brain and spinal cord trauma [33, 68, 95, 144, 175, >>226<<] as discussed earlier." ; ns1:mentions . _:b6628590 rdf:type ns1:Context ; rdf:value "In animal experiments, mild to moderate reactive astrogliosis of this type exhibits the potential for resolution [>>226<<], but the functional consequences of these changes are not well understood." ; ns1:mentions . _:b6628591 rdf:type ns1:Context ; rdf:value "Rather, the concept of the \u2018neurovascular unit\u2019 takes an integrated view of a given brain parenchymal blood vessel and the glial elements that surround it [>>38<<, 139, 206]." ; ns1:mentions . _:b6628592 rdf:type ns1:Context ; rdf:value "Rather, the concept of the \u2018neurovascular unit\u2019 takes an integrated view of a given brain parenchymal blood vessel and the glial elements that surround it [38, >>139<<, 206]. Cellular elements in the vessel wall influence surrounding CNS parenchyma, just as the surrounding parenchymal elements affect vascular morphology and function. The \u2018neurovascular unit\u2019 idea becomes especially important when" ; ns1:mentions . _:b6628593 rdf:type ns1:Context ; rdf:value "Rather, the concept of the \u2018neurovascular unit\u2019 takes an integrated view of a given brain parenchymal blood vessel and the glial elements that surround it [38, 139, >>206<<]. Cellular elements in the vessel wall influence surrounding CNS parenchyma, just as the surrounding parenchymal elements affect vascular morphology and function. The \u2018neurovascular unit\u2019 idea becomes especially important when considering" ; ns1:mentions . _:b6628594 rdf:type ns1:Context ; rdf:value "is at present uncertain, but recent studies suggest that reactive astrocytes provide essential metabolic support to neurons during transient ischemia and that failure of astrocyte functions may contribute to neuronal degeneration [>>196<<, 237]. In addition, experimental disruption of astroglial scar formation in transgenic mice after stroke is associated with loss of barrier functions along the margins of infarcts, resulting in increased spread of inflammation and" ; ns1:mentions . _:b6628595 rdf:type ns1:Context ; rdf:value "is at present uncertain, but recent studies suggest that reactive astrocytes provide essential metabolic support to neurons during transient ischemia and that failure of astrocyte functions may contribute to neuronal degeneration [196, >>237<<]. In addition, experimental disruption of astroglial scar formation in transgenic mice after stroke is associated with loss of barrier functions along the margins of infarcts, resulting in increased spread of inflammation and increased" ; ns1:mentions . _:b6628596 rdf:type ns1:Context ; rdf:value "experimental disruption of astroglial scar formation in transgenic mice after stroke is associated with loss of barrier functions along the margins of infarcts, resulting in increased spread of inflammation and increased lesion volume [>>123<<]." ; ns1:mentions . _:b6628597 rdf:type ns1:Context ; rdf:value "Stroke may also induce neurogenesis from periventricular neural progenitor cells that express GFAP [>>173<<]. Newly \u2018born\u2019 neuroblasts and immature neurons migrate to the infract region where they associate intimately with the cerebral microvasculature in and around the infarct, which itself is undergoing intense post-stroke remodeling." ; ns1:mentions . _:b6628598 rdf:type ns1:Context ; rdf:value "accumulate prominently around microbial abscesses, and recent evidence indicates that reactive astrocytes play essential roles in restricting the spread of invading microbial agents such as Toxoplasma gondii into CNS parenchyma [>>59<<]. These observations are consistent with the putative protective barrier functions of reactive astrocytes to infectious agents and inflammatory cells (Fig." ; ns1:mentions . _:b6628599 rdf:type ns1:Context ; rdf:value "4d) as discussed above and elsewhere [>>226<<]. Reactive astrogliosis can also occur in response to peripheral infections that result in circulating bacterial antigens or endotoxins, such as LPS, due to peritonitis or sepsis without direct CNS infection [105, 213]." ; ns1:mentions . _:b6628600 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis can also occur in response to peripheral infections that result in circulating bacterial antigens or endotoxins, such as LPS, due to peritonitis or sepsis without direct CNS infection [>>105<<, 213]." ; ns1:mentions . _:b6628601 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis can also occur in response to peripheral infections that result in circulating bacterial antigens or endotoxins, such as LPS, due to peritonitis or sepsis without direct CNS infection [105, >>213<<]." ; ns1:mentions . _:b6628602 rdf:type ns1:Context ; rdf:value "Astrocytes are a main target and reservoir of human herpes virus 6 in the CNS, which can cause encephalitis in both healthy and immunsuppressed patients [>>57<<, 222]. Astrocytes are also a main target of human T-lymphotropic virus type-1, leading to disturbances in glutamate homeostasis and excitotoxicity [3, 235]. In addition to being targets of certain viruses, reactive astrocytes may take" ; ns1:mentions . _:b6628603 rdf:type ns1:Context ; rdf:value "Astrocytes are a main target and reservoir of human herpes virus 6 in the CNS, which can cause encephalitis in both healthy and immunsuppressed patients [57, >>222<<]. Astrocytes are also a main target of human T-lymphotropic virus type-1, leading to disturbances in glutamate homeostasis and excitotoxicity [3, 235]. In addition to being targets of certain viruses, reactive astrocytes may take part" ; ns1:mentions . _:b6628604 rdf:type ns1:Context ; rdf:value "Astrocytes are also a main target of human T-lymphotropic virus type-1, leading to disturbances in glutamate homeostasis and excitotoxicity [>>3<<, 235]. In addition to being targets of certain viruses, reactive astrocytes may take part more generally in regulating CNS inflammatory responses [226]. Perivascular cuffing, which is a common and essentially defining feature of different" ; ns1:mentions . _:b6628605 rdf:type ns1:Context ; rdf:value "Astrocytes are also a main target of human T-lymphotropic virus type-1, leading to disturbances in glutamate homeostasis and excitotoxicity [3, >>235<<]. In addition to being targets of certain viruses, reactive astrocytes may take part more generally in regulating CNS inflammatory responses [226]. Perivascular cuffing, which is a common and essentially defining feature of different" ; ns1:mentions . _:b6628606 rdf:type ns1:Context ; rdf:value "In addition to being targets of certain viruses, reactive astrocytes may take part more generally in regulating CNS inflammatory responses [>>226<<]. Perivascular cuffing, which is a common and essentially defining feature of different types of viral encephalitis, may occur as a result of barrier functions of reactive scar forming astrocytes that restrict the spread of inflammatory" ; ns1:mentions . _:b6628607 rdf:type ns1:Context ; rdf:value "1c, d) [>>226<<, 251]. Astrocyte endfeet prominently line blood vessels in healthy tissue (Fig." ; ns1:mentions . _:b6628608 rdf:type ns1:Context ; rdf:value "1c, d) [226, >>251<<]. Astrocyte endfeet prominently line blood vessels in healthy tissue (Fig." ; ns1:mentions . _:b6628609 rdf:type ns1:Context ; rdf:value "1c, d), and experimental disruption of perivascular astrocytes leads to widespread infiltration of lymphocytes and other inflammatory cells into CNS parenchyma [>>251<<].Fig." ; ns1:mentions . _:b6628610 rdf:type ns1:Context ; rdf:value "However, testing of the GFAP gene revealed no mutations (for details, see [>>111<<]). c Comparable section to b showing abundant GFAP immunoreactive astrocytes and associated Rosenthal fibers (arrows). Scale bars a 10\u00A0\u03BCm, b 20\u00A0\u03BCm, c 15" ; ns1:mentions . _:b6628611 rdf:type ns1:Context ; rdf:value "functions, in particular disruption of glutamate homeostasis leading to synapse dysfunction and excitotoxicity are regarded as the most likely mechanisms in mediating HIV related cognitive impairment and neurodegeneration [>>100<<, 253]." ; ns1:mentions . _:b6628612 rdf:type ns1:Context ; rdf:value "Some of the herpes viruses, e.g., Herpes simplex and cytomegalovirus (the latter being a major opportunistic pathogen in the CNS of AIDS patients [>>248<<], infect a wide range of cell types within the CNS including astrocytes, ependyma, and microvascular endothelium." ; ns1:mentions . _:b6628613 rdf:type ns1:Context ; rdf:value "A mosquito-borne flavivirus that has recently appeared in North America, West Nile virus (WNV) infects a variety of tissues throughout the body, but within the CNS appears to favor neurons over astrocytes [>>8<<]. \u2018Neuronotropism\u2019 of viruses is shared by other agents, e.g., the rabies virus, which also appears to spare astrocytes, though the proliferation of uninfected reactive astrocytes is an inevitable result of rabies virus-associated" ; ns1:mentions . _:b6628614 rdf:type ns1:Context ; rdf:value "JC virus may also infect astrocytes, and in situ PCR techniques suggest an even broader repertoire of cells that are vulnerable to JC virus infection [>>132<<, 250]. In this context it is also interesting to note that effector CD8+ T cells form immunological synapses with virally infected astrocytes, resulting in pronounced changes in astrocyte morphology (and presumably in function as well) as" ; ns1:mentions . _:b6628615 rdf:type ns1:Context ; rdf:value "note that effector CD8+ T cells form immunological synapses with virally infected astrocytes, resulting in pronounced changes in astrocyte morphology (and presumably in function as well) as well as potential clearance of infected cells [>>12<<, 13]." ; ns1:mentions . _:b6628616 rdf:type ns1:Context ; rdf:value "that effector CD8+ T cells form immunological synapses with virally infected astrocytes, resulting in pronounced changes in astrocyte morphology (and presumably in function as well) as well as potential clearance of infected cells [12, >>13<<]." ; ns1:mentions . _:b6628617 rdf:type ns1:Context ; rdf:value "astrogliosis is variable, but often prominent, in almost all forms of seizures, and is perhaps most notable in the setting of hippocampal sclerosis, the most common neuropathological substrate of intractable temporal lobe epilepsy [>>64<<]. Astrocytes proliferate in regions of pyramidal neuron loss, usually the endfolium and CA1 segments." ; ns1:mentions . _:b6628618 rdf:type ns1:Context ; rdf:value "In mouse models of severe epilepsy, reactive astrocytes lose their non-overlapping domains and exhibit a tenfold increase in overlapping processes, concurrent with an increase in synaptic spine density [>>169<<]. The nature of reactive astrogliotic changes varies with the intensity and duration of the seizure disorder." ; ns1:mentions . _:b6628619 rdf:type ns1:Context ; rdf:value "techniques guide neurosurgeons to likely \u2018epileptogenic foci\u2019, thereby enabling surgical removal and providing novel lesions for pathologic examination from patients who are relatively \u2018early\u2019 in the course of their epileptic disorder [>>64<<, 150, 152]." ; ns1:mentions . _:b6628620 rdf:type ns1:Context ; rdf:value "guide neurosurgeons to likely \u2018epileptogenic foci\u2019, thereby enabling surgical removal and providing novel lesions for pathologic examination from patients who are relatively \u2018early\u2019 in the course of their epileptic disorder [64, >>150<<, 152]. The neuropathological findings within the foci of cortical dysplasia found in severe intractable epilepsy include pronounced dyslamination of the neocortex, neuronal dysmorphism and massive enlargement (\u2018giant\u2019 neurons)," ; ns1:mentions . _:b6628621 rdf:type ns1:Context ; rdf:value "guide neurosurgeons to likely \u2018epileptogenic foci\u2019, thereby enabling surgical removal and providing novel lesions for pathologic examination from patients who are relatively \u2018early\u2019 in the course of their epileptic disorder [64, 150, >>152<<]. The neuropathological findings within the foci of cortical dysplasia found in severe intractable epilepsy include pronounced dyslamination of the neocortex, neuronal dysmorphism and massive enlargement (\u2018giant\u2019 neurons)," ; ns1:mentions . _:b6628622 rdf:type ns1:Context ; rdf:value "findings within the foci of cortical dysplasia found in severe intractable epilepsy include pronounced dyslamination of the neocortex, neuronal dysmorphism and massive enlargement (\u2018giant\u2019 neurons), gemistocyte-like \u2018balloon cells\u2019 [>>47<<]. Of interest is that some of these cellular elements show immunohistochemical evidence suggesting differentiation along both neuronal and astrocytic lines [47]." ; ns1:mentions . _:b6628623 rdf:type ns1:Context ; rdf:value "Of interest is that some of these cellular elements show immunohistochemical evidence suggesting differentiation along both neuronal and astrocytic lines [>>47<<]. The most severe examples of focal cortical dysplasia (FCD) closely resemble the tubers found within the neocortex of individuals with tuberous sclerosis complex (TSC), and cells within severe FCD or TSC tubers exhibit distinct" ; ns1:mentions . _:b6628624 rdf:type ns1:Context ; rdf:value "FCD or TSC tubers exhibit distinct mechanisms for activating components of insulin-signaling pathways important in cell growth and metabolism, probably reflecting a modulating effect of TSC1 and TSC2 gene products on these pathways [>>152<<, 246]. It is also interesting to note that pronounced astrocytic abnormalities have been described in severe FCD with intractable pediatric epilepsy, including astrocytes with high densities of Rosenthal fibers (Fig." ; ns1:mentions . _:b6628625 rdf:type ns1:Context ; rdf:value "6b, c), comparable to those seen in Alexander\u2019s disease [>>111<<], a genetic disorder with mutation of the GFAP gene that is also associated with seizures and other symptoms (see below)." ; ns1:mentions . _:b6628626 rdf:type ns1:Context ; rdf:value "For example, various antiepileptic therapeutic agents block calcium-signaling in astrocytes [>>240<<]. In mesial temporal lobe epilepsy with hippocampal sclerosis, neuropathological ultrastructural evaluations suggest that reduced levels of AQP4 and dystrophin in perivascular foot-processes of astrocytes and reactive astrocytes may lead" ; ns1:mentions . _:b6628627 rdf:type ns1:Context ; rdf:value "that reduced levels of AQP4 and dystrophin in perivascular foot-processes of astrocytes and reactive astrocytes may lead to perturbed water flux through astrocytes with impaired buffering of K+ and an increased propensity for seizures [>>61<<, 212]. In Rasmussen\u2019s encephalitis, seizures are associated with perivascular reactive astrogliosis and pronounced hypertrophy of astrocyte endfeet (Fig." ; ns1:mentions . _:b6628628 rdf:type ns1:Context ; rdf:value "reduced levels of AQP4 and dystrophin in perivascular foot-processes of astrocytes and reactive astrocytes may lead to perturbed water flux through astrocytes with impaired buffering of K+ and an increased propensity for seizures [61, >>212<<]. In Rasmussen\u2019s encephalitis, seizures are associated with perivascular reactive astrogliosis and pronounced hypertrophy of astrocyte endfeet (Fig." ; ns1:mentions . _:b6628629 rdf:type ns1:Context ; rdf:value "of apparent astrocyte apoptosis and loss, and certain evidence suggests that autoimmune induced (cytotoxic T lymphocyte-mediated) perturbation of astrocyte function and astrocyte degeneration may contribute to the seizure disorder [>>16<<, 256]. Reactive astrocytes may also play a role in focal epilepsy following traumatic, ischemic, or infectious brain injury." ; ns1:mentions . _:b6628630 rdf:type ns1:Context ; rdf:value "of apparent astrocyte apoptosis and loss, and certain evidence suggests that autoimmune induced (cytotoxic T lymphocyte-mediated) perturbation of astrocyte function and astrocyte degeneration may contribute to the seizure disorder [16, >>256<<]. Reactive astrocytes may also play a role in focal epilepsy following traumatic, ischemic, or infectious brain injury." ; ns1:mentions . _:b6628631 rdf:type ns1:Context ; rdf:value "by such insults, exposure of reactive astrocytes to albumin and other serum proteins leads to reduced clearance by reactive astrocytes of synaptic glutamate and K+ that in turn facilitate seizure-like activity and epileptogenesis [>>51<<, 74]." ; ns1:mentions . _:b6628632 rdf:type ns1:Context ; rdf:value "by such insults, exposure of reactive astrocytes to albumin and other serum proteins leads to reduced clearance by reactive astrocytes of synaptic glutamate and K+ that in turn facilitate seizure-like activity and epileptogenesis [51, >>74<<]." ; ns1:mentions . _:b6628633 rdf:type ns1:Context ; rdf:value "plaques of demyelination are interspersed with and surrounded by reactive astrocytes and there are widespread regions of focal reactive astrogliosis of varying intensity throughout white matter and in some regions of gray matter [>>117<<, 130]. Astrocytes in demyelinating disease may exhibit unusual nuclear and cytological features." ; ns1:mentions . _:b6628634 rdf:type ns1:Context ; rdf:value "plaques of demyelination are interspersed with and surrounded by reactive astrocytes and there are widespread regions of focal reactive astrogliosis of varying intensity throughout white matter and in some regions of gray matter [117, >>130<<]. Astrocytes in demyelinating disease may exhibit unusual nuclear and cytological features." ; ns1:mentions . _:b6628635 rdf:type ns1:Context ; rdf:value "Such enlarged multinucleated astrocytes are often referred to as \u2018Creutzfeldt astrocytes\u2019 or \u2018Creutzfeldt\u2013Peters cells\u2019 [>>65<<, 117, 163, 185]." ; ns1:mentions . _:b6628636 rdf:type ns1:Context ; rdf:value "Such enlarged multinucleated astrocytes are often referred to as \u2018Creutzfeldt astrocytes\u2019 or \u2018Creutzfeldt\u2013Peters cells\u2019 [65, >>117<<, 163, 185]." ; ns1:mentions . _:b6628637 rdf:type ns1:Context ; rdf:value "Such enlarged multinucleated astrocytes are often referred to as \u2018Creutzfeldt astrocytes\u2019 or \u2018Creutzfeldt\u2013Peters cells\u2019 [65, 117, >>163<<, 185]. The multiple nuclei within these astrocytes may be fragmented, such that the appearance of a given cell resembles an atypical or \u2018granular mitosis\u2019 of the type often encountered in high grade gliomas. Demyelinating lesions may also" ; ns1:mentions . _:b6628638 rdf:type ns1:Context ; rdf:value "Such enlarged multinucleated astrocytes are often referred to as \u2018Creutzfeldt astrocytes\u2019 or \u2018Creutzfeldt\u2013Peters cells\u2019 [65, 117, 163, >>185<<]. The multiple nuclei within these astrocytes may be fragmented, such that the appearance of a given cell resembles an atypical or \u2018granular mitosis\u2019 of the type often encountered in high grade gliomas. Demyelinating lesions may also" ; ns1:mentions . _:b6628639 rdf:type ns1:Context ; rdf:value "Demyelinating lesions may also exhibit astrocytes that label with markers of cell division [>>45<<]. The obvious diagnostic pitfall here is that a small biopsy from the edge of a demyelinating plaque may suggest a malignancy rather than multiple sclerosis (especially at the time of intraoperative consultation) [45, 65, 163]. Astrocytes" ; ns1:mentions . _:b6628640 rdf:type ns1:Context ; rdf:value "The obvious diagnostic pitfall here is that a small biopsy from the edge of a demyelinating plaque may suggest a malignancy rather than multiple sclerosis (especially at the time of intraoperative consultation) [>>45<<, 65, 163]." ; ns1:mentions . _:b6628641 rdf:type ns1:Context ; rdf:value "The obvious diagnostic pitfall here is that a small biopsy from the edge of a demyelinating plaque may suggest a malignancy rather than multiple sclerosis (especially at the time of intraoperative consultation) [45, >>65<<, 163]. Astrocytes in multiple sclerosis may also demonstrate the phenomenon of \u2018emperipolesis\u2019, i.e., an astrocyte apparently engulfing one or more other cells such as oligodendroglia [81] or lymphocytes [75]. The role of this process in" ; ns1:mentions . _:b6628642 rdf:type ns1:Context ; rdf:value "The obvious diagnostic pitfall here is that a small biopsy from the edge of a demyelinating plaque may suggest a malignancy rather than multiple sclerosis (especially at the time of intraoperative consultation) [45, 65, >>163<<]. Astrocytes in multiple sclerosis may also demonstrate the phenomenon of \u2018emperipolesis\u2019, i.e., an astrocyte apparently engulfing one or more other cells such as oligodendroglia [81] or lymphocytes [75]. The role of this process in the" ; ns1:mentions . _:b6628643 rdf:type ns1:Context ; rdf:value "Astrocytes in multiple sclerosis may also demonstrate the phenomenon of \u2018emperipolesis\u2019, i.e., an astrocyte apparently engulfing one or more other cells such as oligodendroglia [>>81<<] or lymphocytes [75]." ; ns1:mentions . _:b6628644 rdf:type ns1:Context ; rdf:value "Astrocytes in multiple sclerosis may also demonstrate the phenomenon of \u2018emperipolesis\u2019, i.e., an astrocyte apparently engulfing one or more other cells such as oligodendroglia [81] or lymphocytes [>>75<<]. The role of this process in the pathogenesis or progression/chronicity of multiple sclerosis is not certain. It should be emphasized that both multinucleation of astrocytes and astrocyte emperipolesis also occur in other disorders," ; ns1:mentions . _:b6628645 rdf:type ns1:Context ; rdf:value "It should be emphasized that both multinucleation of astrocytes and astrocyte emperipolesis also occur in other disorders, including certain tumors and longstanding spongiform encephalopathy [>>45<<, 81, 155, 217]." ; ns1:mentions . _:b6628646 rdf:type ns1:Context ; rdf:value "It should be emphasized that both multinucleation of astrocytes and astrocyte emperipolesis also occur in other disorders, including certain tumors and longstanding spongiform encephalopathy [45, >>81<<, 155, 217]." ; ns1:mentions . _:b6628647 rdf:type ns1:Context ; rdf:value "It should be emphasized that both multinucleation of astrocytes and astrocyte emperipolesis also occur in other disorders, including certain tumors and longstanding spongiform encephalopathy [45, 81, >>155<<, 217]." ; ns1:mentions . _:b6628648 rdf:type ns1:Context ; rdf:value "It should be emphasized that both multinucleation of astrocytes and astrocyte emperipolesis also occur in other disorders, including certain tumors and longstanding spongiform encephalopathy [45, 81, 155, >>217<<]." ; ns1:mentions . _:b6628649 rdf:type ns1:Context ; rdf:value "Astrocytes can produce a wide variety of pro- or anti-inflammatory molecules [>>58<<, 226], and can exert potent suppressive effects on inflammatory cells [114]." ; ns1:mentions . _:b6628650 rdf:type ns1:Context ; rdf:value "Astrocytes can produce a wide variety of pro- or anti-inflammatory molecules [58, >>226<<], and can exert potent suppressive effects on inflammatory cells [114]." ; ns1:mentions . _:b6628651 rdf:type ns1:Context ; rdf:value "Astrocytes can produce a wide variety of pro- or anti-inflammatory molecules [58, 226], and can exert potent suppressive effects on inflammatory cells [>>114<<]. In the multiple sclerosis like model condition, experimental autoimmune encephalomyelitis (EAE), reactive astrocytes form scar like barriers around perivascular clusters of inflammatory cells (Fig.\u00A01c), and transgenically targeted" ; ns1:mentions . _:b6628652 rdf:type ns1:Context ; rdf:value "1c), and transgenically targeted disruption of these perivascular astrocyte scars in EAE exacerbates the spread of inflammation, increases axonal degeneration, and worsens clinical signs [>>251<<]. Nevertheless, experimental evidence suggests that reactive astrocytes can exert both pro- and anti-inflammatory roles that are essential in EAE [23, 251] and other conditions [226]. While such findings may at first seem at odds with" ; ns1:mentions . _:b6628653 rdf:type ns1:Context ; rdf:value "Nevertheless, experimental evidence suggests that reactive astrocytes can exert both pro- and anti-inflammatory roles that are essential in EAE [>>23<<, 251] and other conditions [226]." ; ns1:mentions . _:b6628654 rdf:type ns1:Context ; rdf:value "Nevertheless, experimental evidence suggests that reactive astrocytes can exert both pro- and anti-inflammatory roles that are essential in EAE [23, >>251<<] and other conditions [226]." ; ns1:mentions . _:b6628655 rdf:type ns1:Context ; rdf:value "Nevertheless, experimental evidence suggests that reactive astrocytes can exert both pro- and anti-inflammatory roles that are essential in EAE [23, 251] and other conditions [>>226<<]. While such findings may at first seem at odds with each other, they may be reconciled by evidence showing that reactive astrocytes take part both in attracting inflammatory cells to specific sites and in restricting inflammatory cells" ; ns1:mentions . _:b6628656 rdf:type ns1:Context ; rdf:value "by evidence showing that reactive astrocytes take part both in attracting inflammatory cells to specific sites and in restricting inflammatory cells to those sites by limiting their spread into adjacent healthy CNS parenchyma [>>226<<]. Such findings further suggest that the loss of normal functions or the gain of abnormal effects by reactive astrocytes may contribute to disease mechanisms in multiple sclerosis and other autoimmune inflammatory conditions." ; ns1:mentions . _:b6628657 rdf:type ns1:Context ; rdf:value "have autoantibodies to aquaporin-4, which is expressed in the CNS only on astrocyte foot processes and that the severity of clinical signs and spinal cord lesions in such patients correlate with aquaporin-4 specific antibody titers [>>119<<, 236]. The potential involvement of astrocytes in other autoimmune inflammatory conditions that sometimes exhibit CNS involvement, such as systemic lupus erythematosus, has been suggested but has not been extensively investigated [242]." ; ns1:mentions . _:b6628658 rdf:type ns1:Context ; rdf:value "autoantibodies to aquaporin-4, which is expressed in the CNS only on astrocyte foot processes and that the severity of clinical signs and spinal cord lesions in such patients correlate with aquaporin-4 specific antibody titers [119, >>236<<]. The potential involvement of astrocytes in other autoimmune inflammatory conditions that sometimes exhibit CNS involvement, such as systemic lupus erythematosus, has been suggested but has not been extensively investigated [242]." ; ns1:mentions . _:b6628659 rdf:type ns1:Context ; rdf:value "The potential involvement of astrocytes in other autoimmune inflammatory conditions that sometimes exhibit CNS involvement, such as systemic lupus erythematosus, has been suggested but has not been extensively investigated [>>242<<]." ; ns1:mentions . _:b6628660 rdf:type ns1:Context ; rdf:value "Although excess uptake of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [>>135<<, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, 177, 264]." ; ns1:mentions . _:b6628661 rdf:type ns1:Context ; rdf:value "Although excess uptake of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, >>157<<, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, 177, 264]." ; ns1:mentions . _:b6628662 rdf:type ns1:Context ; rdf:value "Although excess uptake of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, >>264<<], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, 177, 264]." ; ns1:mentions . _:b6628663 rdf:type ns1:Context ; rdf:value "uptake of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [>>33<<, 157, 177, 264]." ; ns1:mentions . _:b6628664 rdf:type ns1:Context ; rdf:value "of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, >>157<<, 177, 264]." ; ns1:mentions . _:b6628665 rdf:type ns1:Context ; rdf:value "of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, >>177<<, 264]." ; ns1:mentions . _:b6628666 rdf:type ns1:Context ; rdf:value "through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, 177, >>264<<]." ; ns1:mentions . _:b6628667 rdf:type ns1:Context ; rdf:value "role for astrocytes is suggested by studies in transgenic mice in which ablation of reactive astrocytes after CNS trauma prevented the normally occurring repair of the BBB and grafts of normal astrocyte were able to restore BBB repair [>>33<<]. It is not yet known whether a primary dysfunction of astrocytes or reactive astrocytes could lead to loss of BBB integrity." ; ns1:mentions . _:b6628668 rdf:type ns1:Context ; rdf:value "It is possible that loss of astrocyte production of a potential BBB inductive molecule, such as GSNO [>>208<<], or astrocyte over production of BBB disrupting molecules might lead to loss of BBB integrity [69, 188]." ; ns1:mentions . _:b6628669 rdf:type ns1:Context ; rdf:value "It is possible that loss of astrocyte production of a potential BBB inductive molecule, such as GSNO [208], or astrocyte over production of BBB disrupting molecules might lead to loss of BBB integrity [69, >>188<<]." ; ns1:mentions . _:b6628670 rdf:type ns1:Context ; rdf:value "Astrocytes are now recognized as playing a central role in the pathophysiology of hepatic encephalopathy [>>166<<]. The brain edema is largely a result of astrocyte swelling, which in turn is caused by astrocytic uptake of NH4 +. Although astrocyte uptake of NH4 + is regarded initially as a neuroprotective mechanism, it also drives the synthesis of" ; ns1:mentions . _:b6628671 rdf:type ns1:Context ; rdf:value "The accumulation of glutamine in astrocytes also leads to osmotic stress that results in astrocyte swelling and progressive cytotoxic edema [107, >>166<<, 193]." ; ns1:mentions . _:b6628672 rdf:type ns1:Context ; rdf:value "The accumulation of glutamine in astrocytes also leads to osmotic stress that results in astrocyte swelling and progressive cytotoxic edema [107, 166, >>193<<]." ; ns1:mentions . _:b6628673 rdf:type ns1:Context ; rdf:value "processes that are closely associated with nerve terminals, the earliest site of degeneration in the disease, suggesting that disruption of NPC1-mediated vesicular trafficking in astrocytes may be linked to neuronal degeneration [>>178<<]. It is interesting that selective restoration of expression of Npc1 in GFAP-positive astrocytes in Npc1\u2212/\u2212 mice enhanced survival and decreased neuronal storage of cholesterol in the CNS, while restoration of expression of Npc1 in" ; ns1:mentions . _:b6628674 rdf:type ns1:Context ; rdf:value "astrocytes in Npc1\u2212/\u2212 mice enhanced survival and decreased neuronal storage of cholesterol in the CNS, while restoration of expression of Npc1 in GFAP-positive in enteric glial cells in Npc1\u2212/\u2212 mice ameliorated enteric neuropathology [>>110<<, 265]." ; ns1:mentions . _:b6628675 rdf:type ns1:Context ; rdf:value "in Npc1\u2212/\u2212 mice enhanced survival and decreased neuronal storage of cholesterol in the CNS, while restoration of expression of Npc1 in GFAP-positive in enteric glial cells in Npc1\u2212/\u2212 mice ameliorated enteric neuropathology [110, >>265<<]." ; ns1:mentions . _:b6628676 rdf:type ns1:Context ; rdf:value "In the CNS, ceruloplasmin is largely produced by perivascular astrocytes and exhibits a ferroxidase activity that inhibits iron-associated lipid peroxidation and hydroxyl radical formation [>>174<<]. Astrocytes play key roles in iron trafficking and the detoxification of iron-mediated free radicals. Lack of ceruloplasmin causes direct oxidative stress on astrocytes. In aceruloplasminemia, deformed astrocytes accumulate ferric iron" ; ns1:mentions . _:b6628677 rdf:type ns1:Context ; rdf:value "In aceruloplasminemia, deformed astrocytes accumulate ferric iron and the antioxidative ability of astrocytes is compromised, leading to secondary neuronal cell death [>>174<<]." ; ns1:mentions . _:b6628678 rdf:type ns1:Context ; rdf:value "Astrocyte abnormalities and CNS malformations or lesions are also associated with the rare genetic disorders, congenital glutamine synthetase deficiency [>>88<<], and pyruvate carboxylase deficiency [79]." ; ns1:mentions . _:b6628679 rdf:type ns1:Context ; rdf:value "Astrocyte abnormalities and CNS malformations or lesions are also associated with the rare genetic disorders, congenital glutamine synthetase deficiency [88], and pyruvate carboxylase deficiency [>>79<<]." ; ns1:mentions . _:b6628680 rdf:type ns1:Context ; rdf:value "Alexander disease is a genetic disorder of astrocytes caused by a dominant, gain-of-function mutation of the gene encoding GFAP [>>25<<]. Astrocytes are hypertrophied and exhibit numerous, characteristic Rosenthal fibers that are aggregates of GFAP and are therefore prominently GFAP-immunoreactive [25, 247]." ; ns1:mentions . _:b6628681 rdf:type ns1:Context ; rdf:value "Astrocytes are hypertrophied and exhibit numerous, characteristic Rosenthal fibers that are aggregates of GFAP and are therefore prominently GFAP-immunoreactive [>>25<<, 247]. There is particular involvement of the white matter and patients exhibit macrocephaly, seizures, psychomotor disturbances, spasticity, and premature death. Over expression of GFAP in transgenic mice causes a fatal encephalopathy" ; ns1:mentions . _:b6628682 rdf:type ns1:Context ; rdf:value "Over expression of GFAP in transgenic mice causes a fatal encephalopathy similar to the human condition [>>143<<]. It is interesting to note that high densities of Rosenthal fibers, comparable to those seen in Alexander\u2019s disease, have been described in the context of pronounced astrocytic abnormalities in severe FCD with intractable pediatric" ; ns1:mentions . _:b6628683 rdf:type ns1:Context ; rdf:value "to note that high densities of Rosenthal fibers, comparable to those seen in Alexander\u2019s disease, have been described in the context of pronounced astrocytic abnormalities in severe FCD with intractable pediatric epilepsy (Fig.\u00A06b) [>>111<<] (see above)." ; ns1:mentions . _:b6628684 rdf:type ns1:Context ; rdf:value "This localization plus the transmembrane domains of the protein, support the possible transport functions of MLC1, possibly across the blood\u2013brain and brain-cerebrospinal fluid barriers [>>21<<, 210]." ; ns1:mentions . _:b6628685 rdf:type ns1:Context ; rdf:value "This localization plus the transmembrane domains of the protein, support the possible transport functions of MLC1, possibly across the blood\u2013brain and brain-cerebrospinal fluid barriers [21, >>210<<]." ; ns1:mentions . _:b6628686 rdf:type ns1:Context ; rdf:value "of EIF2B5 severely compromised the generation of GFAP expressing astrocytes from normal human glial progenitors, raising the possibility that a deficiency in astrocyte function may contribute to the loss of white matter in VWM [>>55<<, 244]." ; ns1:mentions . _:b6628687 rdf:type ns1:Context ; rdf:value "of EIF2B5 severely compromised the generation of GFAP expressing astrocytes from normal human glial progenitors, raising the possibility that a deficiency in astrocyte function may contribute to the loss of white matter in VWM [55, >>244<<]." ; ns1:mentions . _:b6628688 rdf:type ns1:Context ; rdf:value "the ganglion neurons or whether the gliosis contributes to that degeneration by loss of glial supportive functions, such as glutamate uptake, or contribution of degenerative effects such as production of reactive oxygen species [>>26<<, 109]." ; ns1:mentions . _:b6628689 rdf:type ns1:Context ; rdf:value "the ganglion neurons or whether the gliosis contributes to that degeneration by loss of glial supportive functions, such as glutamate uptake, or contribution of degenerative effects such as production of reactive oxygen species [26, >>109<<]." ; ns1:mentions . _:b6628690 rdf:type ns1:Context ; rdf:value "In rodents, optic nerve astrocytes are spatially aligned to ensheathe axons in bundles in a unique arrangement that provides essential structural support for the axons [>>232<<]. In primates, optic head astrocytes exhibit a similarly specialized morphology and provide additional structural support by secreting an extracellular matrix referred to as the lamina cribrosa [94, 262]. Various lines of evidence suggest" ; ns1:mentions . _:b6628691 rdf:type ns1:Context ; rdf:value "In primates, optic head astrocytes exhibit a similarly specialized morphology and provide additional structural support by secreting an extracellular matrix referred to as the lamina cribrosa [>>94<<, 262]. Various lines of evidence suggest that an early precipitating event in glaucoma may be disturbances of axon\u2013astrocyte interactions at the optic nerve head (perhaps as a consequence of increased stresses caused by raised intraocular" ; ns1:mentions . _:b6628692 rdf:type ns1:Context ; rdf:value "interactions at the optic nerve head (perhaps as a consequence of increased stresses caused by raised intraocular pressure), which in turn lead to axonal damage and subsequent retrograde degeneration of retinal ganglion neurons [>>94<<, 98, 262]." ; ns1:mentions . _:b6628693 rdf:type ns1:Context ; rdf:value "interactions at the optic nerve head (perhaps as a consequence of increased stresses caused by raised intraocular pressure), which in turn lead to axonal damage and subsequent retrograde degeneration of retinal ganglion neurons [94, >>98<<, 262]." ; ns1:mentions . _:b6628694 rdf:type ns1:Context ; rdf:value "Compelling evidence now indicates that pain signaling in the spinal cord dorsal horn involves interactions among microglia, astrocytes and neurons [>>147<<]. As discussed earlier, astrocytes can influence synaptic activity in a variety of direct and indirect ways and astrocytes participate in regulation of CNS inflammation by responding to and producing a wide variety of cytokines." ; ns1:mentions . _:b6628695 rdf:type ns1:Context ; rdf:value "ways, including release of neurotransmitters and neuromodulators such as glutamate, NO and PGE or through release of cytokines like TNF\u03B1 that alter neuronal membrane receptor levels, all of which can amplify neuronal excitability [>>147<<]. The molecules involved in these emerging multi-cellular signaling interactions are providing novel targets for analgesic therapeutic strategies." ; ns1:mentions . _:b6628696 rdf:type ns1:Context ; rdf:value "spreading depression is thought to play a fundamental role in the pathophysiology of migraine and can be caused by excessive synaptic glutamate release, or by decreased removal of glutamate and potassium from the synaptic cleft [>>204<<]. Familial hemiplegic migraine type 2, an autosomal dominant form of migraine with aura, has been associated with four distinct mutations in the alpha2-subunit of the Na+,K+-ATPase that is expressed primarily in astrocytes." ; ns1:mentions . _:b6628697 rdf:type ns1:Context ; rdf:value "The mutations all result in decreased activity of the Na+,K+-pump in astrocytes [>>36<<], which in turn may lower the threshold for cortical spreading depression and migraine attacks." ; ns1:mentions . _:b6628698 rdf:type ns1:Context ; rdf:value "Reactive astrocytes can contain substantial amounts of different forms of amyloid beta, including amyloid beta 1\u201342 (A\u03B242) as well as truncated forms [>>159<<, 239]. Of considerable interest are reports that reactive astrocytes can take up and degrade extracellular deposits of A\u03B242 [261] and that this function is attenuated in ApoE\u2212/\u2212 astrocytes [113], suggesting that reactive astrocytes" ; ns1:mentions . _:b6628699 rdf:type ns1:Context ; rdf:value "Reactive astrocytes can contain substantial amounts of different forms of amyloid beta, including amyloid beta 1\u201342 (A\u03B242) as well as truncated forms [159, >>239<<]. Of considerable interest are reports that reactive astrocytes can take up and degrade extracellular deposits of A\u03B242 [261] and that this function is attenuated in ApoE\u2212/\u2212 astrocytes [113], suggesting that reactive astrocytes functions" ; ns1:mentions . _:b6628700 rdf:type ns1:Context ; rdf:value "Of considerable interest are reports that reactive astrocytes can take up and degrade extracellular deposits of A\u03B242 [>>261<<] and that this function is attenuated in ApoE\u2212/\u2212 astrocytes [113], suggesting that reactive astrocytes functions or dysfunctions could play a role in the progression and severity of AD." ; ns1:mentions . _:b6628701 rdf:type ns1:Context ; rdf:value "Of considerable interest are reports that reactive astrocytes can take up and degrade extracellular deposits of A\u03B242 [261] and that this function is attenuated in ApoE\u2212/\u2212 astrocytes [>>113<<], suggesting that reactive astrocytes functions or dysfunctions could play a role in the progression and severity of AD." ; ns1:mentions . _:b6628702 rdf:type ns1:Context ; rdf:value "Reactive astrocytes also exhibit increased expression of presenilin in sporadic AD [>>101<<, 254], but the consequences of this expression are not known." ; ns1:mentions . _:b6628703 rdf:type ns1:Context ; rdf:value "Reactive astrocytes also exhibit increased expression of presenilin in sporadic AD [101, >>254<<], but the consequences of this expression are not known." ; ns1:mentions . _:b6628704 rdf:type ns1:Context ; rdf:value "3c, 4c), it is not clear whether astrocytes play an active role in prion replication and disease pathogenesis or whether astrogliosis is largely reactive to the disease process in other cell types [>>115<<]. It is interesting that the hippocampal neuronal degeneration associated with experimental ablation of reactive astrocytes has a vacuolar appearance with similarities to spongiform changes [33]." ; ns1:mentions . _:b6628705 rdf:type ns1:Context ; rdf:value "It is interesting that the hippocampal neuronal degeneration associated with experimental ablation of reactive astrocytes has a vacuolar appearance with similarities to spongiform changes [>>33<<]." ; ns1:mentions . _:b6628706 rdf:type ns1:Context ; rdf:value "The role of astrocytes in Parkinson\u2019s disease and related syndromes is sparsely investigated and poorly understood [>>140<<]. Reactive astrogliosis is generally mild or moderate and rarely severe in autopsy specimens of substantia nigra from Parkinson\u2019s disease patients [72, 149]." ; ns1:mentions . _:b6628707 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis is generally mild or moderate and rarely severe in autopsy specimens of substantia nigra from Parkinson\u2019s disease patients [>>72<<, 149]. Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson\u2019s disease. Experimental studies show that astrocytes take up the Parkinson\u2019s syndrome causing molecule, MPTP, from" ; ns1:mentions . _:b6628708 rdf:type ns1:Context ; rdf:value "Reactive astrogliosis is generally mild or moderate and rarely severe in autopsy specimens of substantia nigra from Parkinson\u2019s disease patients [72, >>149<<]. Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson\u2019s disease. Experimental studies show that astrocytes take up the Parkinson\u2019s syndrome causing molecule, MPTP, from the" ; ns1:mentions . _:b6628709 rdf:type ns1:Context ; rdf:value "that astrocytes take up the Parkinson\u2019s syndrome causing molecule, MPTP, from the blood stream and convert it to neurotoxic MPP+ and may similarly convert other environmental molecules that have been implicated in dopaminergic toxicity [>>54<<, 187]. On the other hand, activation of the transcription factor Nrf2 selectively in astrocytes protects mice from MPTP-induced Parkinsonism by activating anti-oxidative response pathways [40]." ; ns1:mentions . _:b6628710 rdf:type ns1:Context ; rdf:value "astrocytes take up the Parkinson\u2019s syndrome causing molecule, MPTP, from the blood stream and convert it to neurotoxic MPP+ and may similarly convert other environmental molecules that have been implicated in dopaminergic toxicity [54, >>187<<]. On the other hand, activation of the transcription factor Nrf2 selectively in astrocytes protects mice from MPTP-induced Parkinsonism by activating anti-oxidative response pathways [40]." ; ns1:mentions . _:b6628711 rdf:type ns1:Context ; rdf:value "On the other hand, activation of the transcription factor Nrf2 selectively in astrocytes protects mice from MPTP-induced Parkinsonism by activating anti-oxidative response pathways [>>40<<]. Rare mutations in Nurr1 lead to familial Parkinson\u2019s disease, and expression of Nurr1 in astrocytes suppresses production of potentially toxic molecules and protects against loss of dopaminergic neurons [203]. Recent findings also show" ; ns1:mentions . _:b6628712 rdf:type ns1:Context ; rdf:value "Rare mutations in Nurr1 lead to familial Parkinson\u2019s disease, and expression of Nurr1 in astrocytes suppresses production of potentially toxic molecules and protects against loss of dopaminergic neurons [>>203<<]. Recent findings also show that subpopulations of astrocytes express disease-related proteins such as \u03B1-synuclein, parkin and phosho-tau to different levels and in different combinations in Parkinson\u2019s disease, multiple-system atrophy," ; ns1:mentions . _:b6628713 rdf:type ns1:Context ; rdf:value "of astrocytes express disease-related proteins such as \u03B1-synuclein, parkin and phosho-tau to different levels and in different combinations in Parkinson\u2019s disease, multiple-system atrophy, and progressive supranuclear palsy [>>227<<], but the roles of astrocytes in these conditions are not yet defined." ; ns1:mentions . _:b6628714 rdf:type ns1:Context ; rdf:value "Sporadic ALS is characterized by selective loss or dysfunction of astrocyte glutamate transporters in spinal cord and cerebral cortical areas that exhibit loss of lower and upper motor neurons [>>73<<, 136, 194, 197], suggesting that increased glutamate excitotoxicity may contribute to motor neuron death and raising the possibility of different types of potential interventions." ; ns1:mentions . _:b6628715 rdf:type ns1:Context ; rdf:value "Sporadic ALS is characterized by selective loss or dysfunction of astrocyte glutamate transporters in spinal cord and cerebral cortical areas that exhibit loss of lower and upper motor neurons [73, >>136<<, 194, 197], suggesting that increased glutamate excitotoxicity may contribute to motor neuron death and raising the possibility of different types of potential interventions." ; ns1:mentions . _:b6628716 rdf:type ns1:Context ; rdf:value "Sporadic ALS is characterized by selective loss or dysfunction of astrocyte glutamate transporters in spinal cord and cerebral cortical areas that exhibit loss of lower and upper motor neurons [73, 136, >>194<<, 197], suggesting that increased glutamate excitotoxicity may contribute to motor neuron death and raising the possibility of different types of potential interventions." ; ns1:mentions . _:b6628717 rdf:type ns1:Context ; rdf:value "Sporadic ALS is characterized by selective loss or dysfunction of astrocyte glutamate transporters in spinal cord and cerebral cortical areas that exhibit loss of lower and upper motor neurons [73, 136, 194, >>197<<], suggesting that increased glutamate excitotoxicity may contribute to motor neuron death and raising the possibility of different types of potential interventions." ; ns1:mentions . _:b6628718 rdf:type ns1:Context ; rdf:value "\u03B2-lactam antibiotics can stimulate the expression of glutamate transporters by astrocyte and thereby enhance glutamate uptake sufficiently to reduce excitotoxicity, and provide neuroprotection in animal models of stroke and ALS [>>199<<]. The \u03B2-lactam antibiotic, Ceftriaxone, began stage 3 clinical trials in May 2009 to determine efficacy in reducing excitotoxicity and neurodegeneration in ALS." ; ns1:mentions . _:b6628719 rdf:type ns1:Context ; rdf:value "Focal grafts of healthy astrocytes are reported to be neuroprotective in an animal model of ALS, suggesting that transplantation of astrocytes may be a potential therapeutic strategy [>>120<<]. From a different perspective, astrocytes may also exhibit neurotoxic dysfunction in ALS. Approximately 20% of familial ALS cases, and about 5% of apparently sporadic cases, exhibit missense mutations of the gene encoding superoxide" ; ns1:mentions . _:b6628720 rdf:type ns1:Context ; rdf:value "Approximately 20% of familial ALS cases, and about 5% of apparently sporadic cases, exhibit missense mutations of the gene encoding superoxide dismutase (SOD) that are dominantly inherited [>>201<<]. Recent findings show that expression of ALS mutant SOD in astrocytes (but not other cell types) leads to production by astrocytes of soluble molecules that are selectively toxic to motor neurons but not to spinal cord interneurons [53," ; ns1:mentions . _:b6628721 rdf:type ns1:Context ; rdf:value "Recent findings show that expression of ALS mutant SOD in astrocytes (but not other cell types) leads to production by astrocytes of soluble molecules that are selectively toxic to motor neurons but not to spinal cord interneurons [>>53<<, 158], but the nature of the toxic molecules and the mechanisms leading to their production are not yet clear." ; ns1:mentions . _:b6628722 rdf:type ns1:Context ; rdf:value "Recent findings show that expression of ALS mutant SOD in astrocytes (but not other cell types) leads to production by astrocytes of soluble molecules that are selectively toxic to motor neurons but not to spinal cord interneurons [53, >>158<<], but the nature of the toxic molecules and the mechanisms leading to their production are not yet clear." ; ns1:mentions . _:b6628723 rdf:type ns1:Context ; rdf:value "Tauopathies are primarily associated with intracellular filamentous deposits in neurons that lead to functional disturbances [>>83<<]. Nevertheless, there is evidence to suggest that astrocyte tau pathology may also contribute to disease mechanisms." ; ns1:mentions . _:b6628724 rdf:type ns1:Context ; rdf:value "Filamentous tau aggregates can be observed in astrocytes in human disease and in animal models, and in animal models can disturb glutamate uptake and other astrocyte functions leading to focal neuronal degeneration [>>48<<, 71]." ; ns1:mentions . _:b6628725 rdf:type ns1:Context ; rdf:value "Filamentous tau aggregates can be observed in astrocytes in human disease and in animal models, and in animal models can disturb glutamate uptake and other astrocyte functions leading to focal neuronal degeneration [48, >>71<<]." ; ns1:mentions . _:b6628726 rdf:type ns1:Context ; rdf:value "In Huntington\u2019s disease, excitotoxicity has long been regarded as contributing to neuronal loss but the underlying mechanisms have been difficult to elucidate [>>82<<]. There is increasing investigation of the potential for astrocytes contributions to dysfunction and degeneration in Huntington\u2019s disease through disturbances in glutamate uptake that can alter synaptic function and lead to" ; ns1:mentions . _:b6628727 rdf:type ns1:Context ; rdf:value "contributions to dysfunction and degeneration in Huntington\u2019s disease through disturbances in glutamate uptake that can alter synaptic function and lead to excitotoxicity, or through abnormal production of neurotoxic molecules [>>127<<, 136]." ; ns1:mentions . _:b6628728 rdf:type ns1:Context ; rdf:value "contributions to dysfunction and degeneration in Huntington\u2019s disease through disturbances in glutamate uptake that can alter synaptic function and lead to excitotoxicity, or through abnormal production of neurotoxic molecules [127, >>136<<]." ; ns1:mentions . _:b6628729 rdf:type ns1:Context ; rdf:value "it becomes increasingly clear that astrocytes play essential roles in synaptic mechanisms (see above), there is growing evidence that astrocyte functions and dysfunctions may contribute to behavioral mechanisms and behavioral disorders [>>90<<]. For example, studies in experimental animals show that disruption of astrocyte-specific Na+,K+-ATPase results in increased anxiety-related behavior and impaired spatial learning in mice [154], and that astrocyte influences on synaptic" ; ns1:mentions . _:b6628730 rdf:type ns1:Context ; rdf:value "For example, studies in experimental animals show that disruption of astrocyte-specific Na+,K+-ATPase results in increased anxiety-related behavior and impaired spatial learning in mice [>>154<<], and that astrocyte influences on synaptic functions are important in reward circuits, and may contribute to drug addiction [145]." ; ns1:mentions . _:b6628731 rdf:type ns1:Context ; rdf:value "Na+,K+-ATPase results in increased anxiety-related behavior and impaired spatial learning in mice [154], and that astrocyte influences on synaptic functions are important in reward circuits, and may contribute to drug addiction [>>145<<]. Clinicopathological studies show that expression of astrocyte glutamate transporters has been found in prefrontal cortex of schizophrenic patients [137], and that the density of astrocytes is reduced in prefrontal cortex of patients" ; ns1:mentions . _:b6628732 rdf:type ns1:Context ; rdf:value "Clinicopathological studies show that expression of astrocyte glutamate transporters has been found in prefrontal cortex of schizophrenic patients [>>137<<], and that the density of astrocytes is reduced in prefrontal cortex of patients with major depressive disorders [146, 189, 218]." ; ns1:mentions . _:b6628733 rdf:type ns1:Context ; rdf:value "that expression of astrocyte glutamate transporters has been found in prefrontal cortex of schizophrenic patients [137], and that the density of astrocytes is reduced in prefrontal cortex of patients with major depressive disorders [>>146<<, 189, 218]." ; ns1:mentions . _:b6628734 rdf:type ns1:Context ; rdf:value "expression of astrocyte glutamate transporters has been found in prefrontal cortex of schizophrenic patients [137], and that the density of astrocytes is reduced in prefrontal cortex of patients with major depressive disorders [146, >>189<<, 218]. Layer-specific reductions in GFAP-reactive have also been reported in astrocytes of the dorsolateral prefrontal cortex in schizophrenia [190] and astrocyte roles in synaptic function are now central to certain hypotheses regarding" ; ns1:mentions . _:b6628735 rdf:type ns1:Context ; rdf:value "of astrocyte glutamate transporters has been found in prefrontal cortex of schizophrenic patients [137], and that the density of astrocytes is reduced in prefrontal cortex of patients with major depressive disorders [146, 189, >>218<<]. Layer-specific reductions in GFAP-reactive have also been reported in astrocytes of the dorsolateral prefrontal cortex in schizophrenia [190] and astrocyte roles in synaptic function are now central to certain hypotheses regarding" ; ns1:mentions . _:b6628736 rdf:type ns1:Context ; rdf:value "Layer-specific reductions in GFAP-reactive have also been reported in astrocytes of the dorsolateral prefrontal cortex in schizophrenia [>>190<<] and astrocyte roles in synaptic function are now central to certain hypotheses regarding schizophrenic disease mechanisms [19, 151]." ; ns1:mentions . _:b6628737 rdf:type ns1:Context ; rdf:value "GFAP-reactive have also been reported in astrocytes of the dorsolateral prefrontal cortex in schizophrenia [190] and astrocyte roles in synaptic function are now central to certain hypotheses regarding schizophrenic disease mechanisms [>>19<<, 151]." ; ns1:mentions . _:b6628738 rdf:type ns1:Context ; rdf:value "have also been reported in astrocytes of the dorsolateral prefrontal cortex in schizophrenia [190] and astrocyte roles in synaptic function are now central to certain hypotheses regarding schizophrenic disease mechanisms [19, >>151<<]." ; ns1:mentions . _:b6628739 rdf:type ns1:Context ; rdf:value "Malignant astrocytic glioma, such as glioblastoma (astrocytoma WHO grade IV), are the most common and among the most lethal intracranial tumors [>>76<<, 128]. The cells of origin of astrocytic gliomas, whether potentially astrocytes, glial precursors, or stem cells, are the subject of intense investigation [76]." ; ns1:mentions . _:b6628740 rdf:type ns1:Context ; rdf:value "Malignant astrocytic glioma, such as glioblastoma (astrocytoma WHO grade IV), are the most common and among the most lethal intracranial tumors [76, >>128<<]. The cells of origin of astrocytic gliomas, whether potentially astrocytes, glial precursors, or stem cells, are the subject of intense investigation [76]." ; ns1:mentions . _:b6628741 rdf:type ns1:Context ; rdf:value "The cells of origin of astrocytic gliomas, whether potentially astrocytes, glial precursors, or stem cells, are the subject of intense investigation [>>76<<]. In a manner consistent with the cancer stem cell hypothesis, there is considerable evidence that only minor populations of cells in primary gliomas are capable of forming a tumor, [76, 223]. The presence throughout adult brain of" ; ns1:mentions . _:b6628742 rdf:type ns1:Context ; rdf:value "In a manner consistent with the cancer stem cell hypothesis, there is considerable evidence that only minor populations of cells in primary gliomas are capable of forming a tumor, [>>76<<, 223]. The presence throughout adult brain of periventricular adult NSC that express the astrocyte marker GFAP (see above), raises interesting questions regarding the possible contribution of these cells to astrocytoma initiation." ; ns1:mentions . _:b6628743 rdf:type ns1:Context ; rdf:value "In a manner consistent with the cancer stem cell hypothesis, there is considerable evidence that only minor populations of cells in primary gliomas are capable of forming a tumor, [76, >>223<<]. The presence throughout adult brain of periventricular adult NSC that express the astrocyte marker GFAP (see above), raises interesting questions regarding the possible contribution of these cells to astrocytoma initiation. Astrocytic" ; ns1:mentions . _:b6628744 rdf:type ns1:Context ; rdf:value "contain small numbers of cells that exhibit stem cell-like properties in that they self-renew, are multipotent and form neurospheres in vitro and constitutively produce the different types of cells found within the parent tumors [>>160<<]. Growth properties of glioma-derived neurospheres in vitro were found to be significant predictors of tumor progression in vivo and of clinical outcome [118]." ; ns1:mentions . _:b6628745 rdf:type ns1:Context ; rdf:value "Growth properties of glioma-derived neurospheres in vitro were found to be significant predictors of tumor progression in vivo and of clinical outcome [>>118<<]. Nevertheless, the origins of glioma are not yet understood and could be heterogeneous. Astrocytic gliomas exhibit molecular heterogeneity, particularly as regards expression patterns of transcriptional regulators, tumor-suppressor" ; ns1:mentions . _:b6628746 rdf:type ns1:Context ; rdf:value "particularly as regards expression patterns of transcriptional regulators, tumor-suppressor proteins and kinase mutations, and molecular phenotyping of glioma is opening up the potential for molecularly targeted therapies [>>99<<]. Some properties of astroglioma appear related to astrocyte functions. For example, glutamate production by glioma may increase invasive growth properties [228]." ; ns1:mentions . _:b6628747 rdf:type ns1:Context ; rdf:value "For example, glutamate production by glioma may increase invasive growth properties [>>228<<]. Enhanced STAT3 signaling activity by astroglioma reduces inflammation and tumor-immune surveillance and increases cell proliferation [24] in a manner consistent with functions of STAT3 signaling in astrocytes [95]." ; ns1:mentions . _:b6628748 rdf:type ns1:Context ; rdf:value "Enhanced STAT3 signaling activity by astroglioma reduces inflammation and tumor-immune surveillance and increases cell proliferation [>>24<<] in a manner consistent with functions of STAT3 signaling in astrocytes [95]." ; ns1:mentions . _:b6628749 rdf:type ns1:Context ; rdf:value "Enhanced STAT3 signaling activity by astroglioma reduces inflammation and tumor-immune surveillance and increases cell proliferation [24] in a manner consistent with functions of STAT3 signaling in astrocytes [>>95<<]." ; ns1:mentions . _:b6628750 rdf:type ns1:Context ; rdf:value "Neurofibromatosis type 1 (NF1) is an inherited neurocutaneous disorder with neuropsychologic deficits and predisposition to Schwannomas and astrocytomas caused by mutations in the NF1 gene [>>2<<, 9]. Reduced expression of glutamate transporters have been reported in reactive astrocyte clusters in NF1 [263]." ; ns1:mentions . _:b6628751 rdf:type ns1:Context ; rdf:value "Neurofibromatosis type 1 (NF1) is an inherited neurocutaneous disorder with neuropsychologic deficits and predisposition to Schwannomas and astrocytomas caused by mutations in the NF1 gene [2, >>9<<]. Reduced expression of glutamate transporters have been reported in reactive astrocyte clusters in NF1 [263]." ; ns1:mentions . _:b6628752 rdf:type ns1:Context ; rdf:value "Reduced expression of glutamate transporters have been reported in reactive astrocyte clusters in NF1 [>>263<<]. Changes in mTOR and PTEN-signaling pathways in Schwann cells and astrocytes may contribute to tumorigenesis in NF1 [50, 87]." ; ns1:mentions . _:b6628753 rdf:type ns1:Context ; rdf:value "Changes in mTOR and PTEN-signaling pathways in Schwann cells and astrocytes may contribute to tumorigenesis in NF1 [>>50<<, 87]." ; ns1:mentions . _:b6628754 rdf:type ns1:Context ; rdf:value "glia populates gut muscle layers and the intestinal mucosa, and mounting new evidence points toward enteric glia, which express GFAP and share functional similarities with astrocytes, as active participants in gut pathology [>>207<<]. Various lines of experimental and neuropathological evidence are consistent with the possibility that enteric glia constitute a previously unrecognized disease target in pathologies associated with intestinal barrier dysfunction," ; ns1:mentions . _:b6628755 rdf:type ns1:Context ; rdf:value "in pathologies associated with intestinal barrier dysfunction, notably inflammatory bowel disease, necrotizing enterocolitis, irritable bowel syndrome, diabetes, autoimmune disease, and neurotropic virus infection of the gut pathology [>>44<<, 207]. Experimental ablation of enteric glia leads to inflammatory bowel disease [32]." ; ns1:mentions . _:b6628756 rdf:type ns1:Context ; rdf:value "associated with intestinal barrier dysfunction, notably inflammatory bowel disease, necrotizing enterocolitis, irritable bowel syndrome, diabetes, autoimmune disease, and neurotropic virus infection of the gut pathology [44, >>207<<]. Experimental ablation of enteric glia leads to inflammatory bowel disease [32]." ; ns1:mentions . _:b6628757 rdf:type ns1:Context ; rdf:value "Experimental ablation of enteric glia leads to inflammatory bowel disease [>>32<<]. Both astrocytes and related enteric glial cells are able to induce barrier properties in gut epithelial cells, and S-nitrosoglutathione (GSNO) has been identified as one molecular mediator of this effect [208]." ; ns1:mentions . _:b6628758 rdf:type ns1:Context ; rdf:value "Both astrocytes and related enteric glial cells are able to induce barrier properties in gut epithelial cells, and S-nitrosoglutathione (GSNO) has been identified as one molecular mediator of this effect [>>208<<]. Thus, enteric glia, like astrocytes, appear to play essential roles in barrier functions during disease processes, particularly as regards regulating the spread of inflammation [49, 207, 226, 251]." ; ns1:mentions . _:b6628759 rdf:type ns1:Context ; rdf:value "Thus, enteric glia, like astrocytes, appear to play essential roles in barrier functions during disease processes, particularly as regards regulating the spread of inflammation [49, >>207<<, 226, 251]." ; ns1:mentions . _:b6628760 rdf:type ns1:Context ; rdf:value "Thus, enteric glia, like astrocytes, appear to play essential roles in barrier functions during disease processes, particularly as regards regulating the spread of inflammation [49, 207, >>226<<, 251]." ; ns1:mentions . _:b6628761 rdf:type ns1:Context ; rdf:value "Thus, enteric glia, like astrocytes, appear to play essential roles in barrier functions during disease processes, particularly as regards regulating the spread of inflammation [49, 207, 226, >>251<<]." ; ns1:mentions . _:b6628762 rdf:type ns1:Context ; rdf:value "For example, there is increasing evidence that GFAP-expressing pancreatic stellate cells play important roles in tissue repair, fibrosis, and scar formation [>>176<<]. Hepatic stellate cells not only express GFAP and have morphological appearance similar to astrocytes, but also contact hepatic sinusoids and blood vessels and may take part in hepatic immune processes [258, 259]. In this regard, it is" ; ns1:mentions . _:b6628763 rdf:type ns1:Context ; rdf:value "Hepatic stellate cells not only express GFAP and have morphological appearance similar to astrocytes, but also contact hepatic sinusoids and blood vessels and may take part in hepatic immune processes [>>258<<, 259]. In this regard, it is particularly interesting that the liver, like the CNS, has a certain level of immune privilege [241], and that both CNS and liver have resident populations of macrophage-related cells (Kupfer cells in the" ; ns1:mentions . _:b6628764 rdf:type ns1:Context ; rdf:value "Hepatic stellate cells not only express GFAP and have morphological appearance similar to astrocytes, but also contact hepatic sinusoids and blood vessels and may take part in hepatic immune processes [258, >>259<<]. In this regard, it is particularly interesting that the liver, like the CNS, has a certain level of immune privilege [241], and that both CNS and liver have resident populations of macrophage-related cells (Kupfer cells in the liver and" ; ns1:mentions . _:b6628765 rdf:type ns1:Context ; rdf:value "In addition, there is evidence that GFAP-expressing mesangial cells in the kidney function as local modulators of innate and adaptive immune responses [>>209<<]. The increasing recognition that tissue-specific cells like astrocytes and stellate cells play essential roles in regulating local immune and inflammatory processes is likely to impact considerably on concepts about organ-specific" ; ns1:mentions . _:b6628766 rdf:type ns1:Context ; rdf:value "The actively ongoing dissection of molecular mechanisms of reactive astrogliosis is beginning to identify molecules whose functions might be enhanced or blocked in specific disease contexts as potential therapeutic strategies [>>66<<, 226]. For example, augmenting the function of the astrocyte glutamate transporter EAAT2 with parawexin 1, a molecule isolated from spider venom, protects retinal neurons from ischemic degeneration by enhancing glutamate uptake and" ; ns1:mentions . _:b6628767 rdf:type ns1:Context ; rdf:value "The actively ongoing dissection of molecular mechanisms of reactive astrogliosis is beginning to identify molecules whose functions might be enhanced or blocked in specific disease contexts as potential therapeutic strategies [66, >>226<<]. For example, augmenting the function of the astrocyte glutamate transporter EAAT2 with parawexin 1, a molecule isolated from spider venom, protects retinal neurons from ischemic degeneration by enhancing glutamate uptake and reducing" ; ns1:mentions . _:b6628768 rdf:type ns1:Context ; rdf:value "augmenting the function of the astrocyte glutamate transporter EAAT2 with parawexin 1, a molecule isolated from spider venom, protects retinal neurons from ischemic degeneration by enhancing glutamate uptake and reducing excitotoxicity [>>70<<]. Certain \u03B2-lactam antibiotics, identified by a high-throughput screen of small molecules, can stimulate the expression of astrocyte glutamate transporters sufficiently to reduce excitotoxicity and neuroprotection in models of stroke and" ; ns1:mentions . _:b6628769 rdf:type ns1:Context ; rdf:value "\u03B2-lactam antibiotics, identified by a high-throughput screen of small molecules, can stimulate the expression of astrocyte glutamate transporters sufficiently to reduce excitotoxicity and neuroprotection in models of stroke and ALS [>>199<<]." ; ns1:mentions . _:b6628770 rdf:type ns1:Context ; rdf:value "For example, grafts of stem or progenitor cells that mature into healthy astrocytes cells are reported to improve outcome in a mouse model of ALS in which host astrocytes are abnormal and express a mutant SOD [>>120<<]. A different strategy employs grafts of astrocytes that are genetically modified to produce specific molecules, such as growth factors, as therapeutic pumps to deliver those molecules in specific locations [18, 233]. In due course," ; ns1:mentions . _:b6628771 rdf:type ns1:Context ; rdf:value "A different strategy employs grafts of astrocytes that are genetically modified to produce specific molecules, such as growth factors, as therapeutic pumps to deliver those molecules in specific locations [>>18<<, 233]. In due course, grafted astrocytes may be tested in clinical contexts and become subject to neuropathological evaluations." ; ns1:mentions . _:b6628772 rdf:type ns1:Context ; rdf:value "A different strategy employs grafts of astrocytes that are genetically modified to produce specific molecules, such as growth factors, as therapeutic pumps to deliver those molecules in specific locations [18, >>233<<]. 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