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n2:pmcid
PMC0
bibo:doi
10.1007%2Fs12035-013-8620-6
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_:vb27794883 _:vb27794900 _:vb27794942
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_:vb27794883
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n6:Section
dc:title
introduction
n6:contains
_:vb27794888 _:vb27794889 _:vb27794890 _:vb27794891 _:vb27794892 _:vb27794893 _:vb27794894 _:vb27794895 _:vb27794884 _:vb27794885 _:vb27794886 _:vb27794887 _:vb27794896 _:vb27794897 _:vb27794898 _:vb27794899
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_:vb27794884
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In response to injury or pathogen invasion however, microglia transform into active phagocytic microglia [>>1<<], migrate, and accumulate at the site of injury through a process known as chemotaxis [2].
n2:mentions
n3:11241743
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_:vb27794885
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In response to injury or pathogen invasion however, microglia transform into active phagocytic microglia [1], migrate, and accumulate at the site of injury through a process known as chemotaxis [>>2<<]. Being different to their resting phenotype, activated microglia are identified by their retracted processes and “amoeboid” morphology, release of both pro- and anti-inflammatory molecules, and high capacity for phagocytic removal of
n2:mentions
n3:11259646
Subject Item
_:vb27794886
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resting phenotype, activated microglia are identified by their retracted processes and “amoeboid” morphology, release of both pro- and anti-inflammatory molecules, and high capacity for phagocytic removal of apoptotic cells and debris [>>3<<, 4]. Activated microglia are observed in nearly all kinds of neurological diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7];
n2:mentions
n3:7550361
Subject Item
_:vb27794887
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n2:Context
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phenotype, activated microglia are identified by their retracted processes and “amoeboid” morphology, release of both pro- and anti-inflammatory molecules, and high capacity for phagocytic removal of apoptotic cells and debris [3, >>4<<]. Activated microglia are observed in nearly all kinds of neurological diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7];
n2:mentions
n3:18567623
Subject Item
_:vb27794888
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rdf:value
Activated microglia are observed in nearly all kinds of neurological diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [>>5<<], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [10]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:24224195
Subject Item
_:vb27794889
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n2:Context
rdf:value
Activated microglia are observed in nearly all kinds of neurological diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [>>6<<], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [10]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:19686799
Subject Item
_:vb27794890
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Activated microglia are observed in nearly all kinds of neurological diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [>>7<<]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [10]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:15846792
Subject Item
_:vb27794891
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diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [>>8<<, 9]; stroke [10]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:19409897
Subject Item
_:vb27794892
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diseases, including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, >>9<<]; stroke [10]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:11455614
Subject Item
_:vb27794893
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including neurodegenerative diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [>>10<<]; and traumatic [11] and radiation-induced brain injury [12].
n2:mentions
n3:20880502
Subject Item
_:vb27794894
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diseases such as Alzheimer’s disease (AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [10]; and traumatic [>>11<<] and radiation-induced brain injury [12].
n2:mentions
n3:20880501
Subject Item
_:vb27794895
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(AD) [5], Parkinson’s disease (PD) [6], and amyotrophic lateral sclerosis (ALS) [7]; infectious and inflammatory diseases such as multiple sclerosis (MS) [8, 9]; stroke [10]; and traumatic [11] and radiation-induced brain injury [>>12<<].
n2:mentions
n3:8295989
Subject Item
_:vb27794896
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Recently, “phagoptosis” has been proposed as a form of cell death, caused by phagocytosis of viable cells [>>13<<]. It is also known as “primary phagocytosis.” It is provoked by exposure of “eat-me” signals and/or loss of “don’t-eat-me” signals by viable cells, causing their phagocytosis by phagocytes and resulting in self-destruction [13].
n2:mentions
n3:22682109
Subject Item
_:vb27794897
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” It is provoked by exposure of “eat-me” signals and/or loss of “don’t-eat-me” signals by viable cells, causing their phagocytosis by phagocytes and resulting in self-destruction [>>13<<]. Phagocytosis is normally exerted by phagocytic cells, such as microglia and macrophages [13]. Whether microglial phagocytosis plays a beneficial or detrimental role in brain diseases remains controversial, though most researchers are in
n2:mentions
n3:22682109
Subject Item
_:vb27794898
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Phagocytosis is normally exerted by phagocytic cells, such as microglia and macrophages [>>13<<]. Whether microglial phagocytosis plays a beneficial or detrimental role in brain diseases remains controversial, though most researchers are in favor of the former claim since efficient clearance of tissue debris is critical in
n2:mentions
n3:22682109
Subject Item
_:vb27794899
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diseases remains controversial, though most researchers are in favor of the former claim since efficient clearance of tissue debris is critical in reconstruction and reorganization of neuronal networking after an injury in the brain [>>14<<–16]. The crucial beneficial role of microglial phagocytosis in axon regeneration and in restoration of the microenvironment has also been shown during the recovery of an acute brain injury.
n2:mentions
n3:20887954 n3:17673709 n3:9482801
Subject Item
_:vb27794900
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n6:Section
dc:title
receptors involved in microglial phagocytosis
n6:contains
_:vb27794932 _:vb27794933 _:vb27794934 _:vb27794935 _:vb27794928 _:vb27794929 _:vb27794930 _:vb27794931 _:vb27794940 _:vb27794941 _:vb27794936 _:vb27794937 _:vb27794938 _:vb27794939 _:vb27794916 _:vb27794917 _:vb27794918 _:vb27794919 _:vb27794912 _:vb27794913 _:vb27794914 _:vb27794915 _:vb27794924 _:vb27794925 _:vb27794926 _:vb27794927 _:vb27794920 _:vb27794921 _:vb27794922 _:vb27794923 _:vb27794901 _:vb27794902 _:vb27794903 _:vb27794908 _:vb27794909 _:vb27794910 _:vb27794911 _:vb27794904 _:vb27794905 _:vb27794906 _:vb27794907
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_:vb27794901
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Microglial phagocytosis may need different types of receptors to initiate function [>>17<<]. In general, there are two distinctive types of receptors, one with a high affinity to bind to foreign microbial pathogens, such as Toll-like receptors (TLRs), and another recognizing apoptotic cellular substances, such as triggering
n2:mentions
n3:10358769
Subject Item
_:vb27794902
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Besides these two types, some receptors including Fc receptors, complement receptors [>>18<<], scavenger receptors (SR), pyrimidinergic receptor P2Y, G-protein coupled, 6 (P2RY6), macrophage antigen complex 2 (MAC-2), mannose receptor [19], and low-density lipoprotein receptor-related protein (LRP) receptor also participate in
n2:mentions
n3:21546088
Subject Item
_:vb27794903
rdf:type
n2:Context
rdf:value
Besides these two types, some receptors including Fc receptors, complement receptors [18], scavenger receptors (SR), pyrimidinergic receptor P2Y, G-protein coupled, 6 (P2RY6), macrophage antigen complex 2 (MAC-2), mannose receptor [>>19<<], and low-density lipoprotein receptor-related protein (LRP) receptor also participate in microglial clearance of misfolded, apoptotic cells and dead neurons in both acute and chronic brain injury [20].
n2:mentions
n3:19840553
Subject Item
_:vb27794904
rdf:type
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2 (MAC-2), mannose receptor [19], and low-density lipoprotein receptor-related protein (LRP) receptor also participate in microglial clearance of misfolded, apoptotic cells and dead neurons in both acute and chronic brain injury [>>20<<].Fig.
n2:mentions
n3:9972873
Subject Item
_:vb27794905
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ReceptorsStimulusCell types expressedDiseases/animal modelsReferencesTLRsα-SynucleinMicrogliaalpha-Synucleinopathies, Alzheimer’s disease[>>23<<, 120–122]Fibrillar AβAstrocytesBacterial strainsOligodendrocytesCNS infections, spinal cord injury, and neuronal injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[34, 123]MacrophagesNasu-Hakola diseaseMonocyte-derived
n2:mentions
n3:21745188
Subject Item
_:vb27794906
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ReceptorsStimulusCell types expressedDiseases/animal modelsReferencesTLRsα-SynucleinMicrogliaalpha-Synucleinopathies, Alzheimer’s disease[23, >>120<<–122]Fibrillar AβAstrocytesBacterial strainsOligodendrocytesCNS infections, spinal cord injury, and neuronal injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[34, 123]MacrophagesNasu-Hakola diseaseMonocyte-derived dendritic
n2:mentions
n3:21827663 n3:23108585 n3:19780198
Subject Item
_:vb27794907
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Alzheimer’s disease[23, 120–122]Fibrillar AβAstrocytesBacterial strainsOligodendrocytesCNS infections, spinal cord injury, and neuronal injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[>>34<<, 123]MacrophagesNasu-Hakola diseaseMonocyte-derived dendritic cellsMultiple sclerosis/EAEOsteoclastsFc receptors (FcγR)α-SynucleinNeuronsParkinson’s disease[124, 125]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s
n2:mentions
n3:17407101
Subject Item
_:vb27794908
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Alzheimer’s disease[23, 120–122]Fibrillar AβAstrocytesBacterial strainsOligodendrocytesCNS infections, spinal cord injury, and neuronal injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[34, >>123<<]MacrophagesNasu-Hakola diseaseMonocyte-derived dendritic cellsMultiple sclerosis/EAEOsteoclastsFc receptors (FcγR)α-SynucleinNeuronsParkinson’s disease[124, 125]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s
n2:mentions
n3:23208114
Subject Item
_:vb27794909
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n2:Context
rdf:value
neuronal injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[34, 123]MacrophagesNasu-Hakola diseaseMonocyte-derived dendritic cellsMultiple sclerosis/EAEOsteoclastsFc receptors (FcγR)α-SynucleinNeuronsParkinson’s disease[>>124<<, 125]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s diseaseOligodendrocytesComplement receptors (CR3 (CD11b/CD18), CR4 (CD11c/CD18))Degenerated myelinMicrogliaAlzheimer’s disease[126, 127]AβMacrophagesWallerian degenerationApoptotic
n2:mentions
n3:19844812
Subject Item
_:vb27794910
rdf:type
n2:Context
rdf:value
injuryLPSNeuronsTREM-2Amyloid proteinMicrogliaAlzheimer’s disease[34, 123]MacrophagesNasu-Hakola diseaseMonocyte-derived dendritic cellsMultiple sclerosis/EAEOsteoclastsFc receptors (FcγR)α-SynucleinNeuronsParkinson’s disease[124, >>125<<]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s diseaseOligodendrocytesComplement receptors (CR3 (CD11b/CD18), CR4 (CD11c/CD18))Degenerated myelinMicrogliaAlzheimer’s disease[126, 127]AβMacrophagesWallerian degenerationApoptotic
n2:mentions
n3:23186369
Subject Item
_:vb27794911
rdf:type
n2:Context
rdf:value
(FcγR)α-SynucleinNeuronsParkinson’s disease[124, 125]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s diseaseOligodendrocytesComplement receptors (CR3 (CD11b/CD18), CR4 (CD11c/CD18))Degenerated myelinMicrogliaAlzheimer’s disease[>>126<<, 127]AβMacrophagesWallerian degenerationApoptotic cellsMultiple sclerosisScavenger receptors (SR-A, SR-BI, CD36, RAGE)Degenerated myelinMicroglia, astrocytes, mato cells, cerebral microvascular endothelial cells, cerebral arterial smooth
n2:mentions
n3:11578768
Subject Item
_:vb27794912
rdf:type
n2:Context
rdf:value
(FcγR)α-SynucleinNeuronsParkinson’s disease[124, 125]AstrocytesMultiple sclerosisMicrogliaAlzheimer’s diseaseOligodendrocytesComplement receptors (CR3 (CD11b/CD18), CR4 (CD11c/CD18))Degenerated myelinMicrogliaAlzheimer’s disease[126, >>127<<]AβMacrophagesWallerian degenerationApoptotic cellsMultiple sclerosisScavenger receptors (SR-A, SR-BI, CD36, RAGE)Degenerated myelinMicroglia, astrocytes, mato cells, cerebral microvascular endothelial cells, cerebral arterial smooth
n2:mentions
n3:22776089
Subject Item
_:vb27794913
rdf:type
n2:Context
rdf:value
receptors (SR-A, SR-BI, CD36, RAGE)Degenerated myelinMicroglia, astrocytes, mato cells, cerebral microvascular endothelial cells, cerebral arterial smooth muscle cells, retinal pigment epithelial cellsMultiple sclerosis/EAE[>>128<<–131]fAβ, thrombospondin-1Amyotrophic lateral sclerosisAnionic polysaccharideAlzheimer’s diseasePolynucleotidesChemically modified proteinsApoptotic cellsBacteriaP2RY6ATP and other nucleotidesMicrogliaNeuropathic pain[37,
n2:mentions
n3:23334594 n3:23281114 n3:12379907 n3:15987691
Subject Item
_:vb27794914
rdf:type
n2:Context
rdf:value
sclerosis/EAE[128–131]fAβ, thrombospondin-1Amyotrophic lateral sclerosisAnionic polysaccharideAlzheimer’s diseasePolynucleotidesChemically modified proteinsApoptotic cellsBacteriaP2RY6ATP and other nucleotidesMicrogliaNeuropathic pain[>>37<<, 132]Galectin-3/MAC-2Degenerated myelinMicrogliaTraumatic brain injury[133, 134]MacrophagesSpinal cord injurySchwann cellsMultiple sclerosis/EAELRP receptors (low-density lipoprotein receptor-related protein-1)LPS or AβNeuronsAlzheimer’s
n2:mentions
n3:17410128
Subject Item
_:vb27794915
rdf:type
n2:Context
rdf:value
thrombospondin-1Amyotrophic lateral sclerosisAnionic polysaccharideAlzheimer’s diseasePolynucleotidesChemically modified proteinsApoptotic cellsBacteriaP2RY6ATP and other nucleotidesMicrogliaNeuropathic pain[37, >>132<<]Galectin-3/MAC-2Degenerated myelinMicrogliaTraumatic brain injury[133, 134]MacrophagesSpinal cord injurySchwann cellsMultiple sclerosis/EAELRP receptors (low-density lipoprotein receptor-related protein-1)LPS or AβNeuronsAlzheimer’s
n2:mentions
n3:22736439
Subject Item
_:vb27794916
rdf:type
n2:Context
rdf:value
polysaccharideAlzheimer’s diseasePolynucleotidesChemically modified proteinsApoptotic cellsBacteriaP2RY6ATP and other nucleotidesMicrogliaNeuropathic pain[37, 132]Galectin-3/MAC-2Degenerated myelinMicrogliaTraumatic brain injury[>>133<<, 134]MacrophagesSpinal cord injurySchwann cellsMultiple sclerosis/EAELRP receptors (low-density lipoprotein receptor-related protein-1)LPS or AβNeuronsAlzheimer’s disease[135–137]Brain capillary endotheliumPhosphatidylserine receptors
n2:mentions
n3:19253007
Subject Item
_:vb27794917
rdf:type
n2:Context
rdf:value
polysaccharideAlzheimer’s diseasePolynucleotidesChemically modified proteinsApoptotic cellsBacteriaP2RY6ATP and other nucleotidesMicrogliaNeuropathic pain[37, 132]Galectin-3/MAC-2Degenerated myelinMicrogliaTraumatic brain injury[133, >>134<<]MacrophagesSpinal cord injurySchwann cellsMultiple sclerosis/EAELRP receptors (low-density lipoprotein receptor-related protein-1)LPS or AβNeuronsAlzheimer’s disease[135–137]Brain capillary endotheliumPhosphatidylserine receptors
n2:mentions
n3:10619568
Subject Item
_:vb27794918
rdf:type
n2:Context
rdf:value
myelinMicrogliaTraumatic brain injury[133, 134]MacrophagesSpinal cord injurySchwann cellsMultiple sclerosis/EAELRP receptors (low-density lipoprotein receptor-related protein-1)LPS or AβNeuronsAlzheimer’s disease[>>135<<–137]Brain capillary endotheliumPhosphatidylserine receptors (phosphatidyl-serine-specific receptor)Apoptotic and necrotic neuronsMacrophagesAlzheimer’s disease[138, 139]FibroblastsEpithelial cellsDendritic cellsMannose receptorsSoluble
n2:mentions
n3:10797543 n3:18673201 n3:22889139
Subject Item
_:vb27794919
rdf:type
n2:Context
rdf:value
receptor-related protein-1)LPS or AβNeuronsAlzheimer’s disease[135–137]Brain capillary endotheliumPhosphatidylserine receptors (phosphatidyl-serine-specific receptor)Apoptotic and necrotic neuronsMacrophagesAlzheimer’s disease[>>138<<, 139]FibroblastsEpithelial cellsDendritic cellsMannose receptorsSoluble immune components, cell debris, cytotoxic substances, myelin glycoproteins, degrading enzymes, microbial ligandsAstrocytesIschemia[140,
n2:mentions
n3:15126686
Subject Item
_:vb27794920
rdf:type
n2:Context
rdf:value
receptor-related protein-1)LPS or AβNeuronsAlzheimer’s disease[135–137]Brain capillary endotheliumPhosphatidylserine receptors (phosphatidyl-serine-specific receptor)Apoptotic and necrotic neuronsMacrophagesAlzheimer’s disease[138, >>139<<]FibroblastsEpithelial cellsDendritic cellsMannose receptorsSoluble immune components, cell debris, cytotoxic substances, myelin glycoproteins, degrading enzymes, microbial ligandsAstrocytesIschemia[140, 141]PerivascularMeningealChoroid
n2:mentions
n3:14502239
Subject Item
_:vb27794921
rdf:type
n2:Context
rdf:value
disease[138, 139]FibroblastsEpithelial cellsDendritic cellsMannose receptorsSoluble immune components, cell debris, cytotoxic substances, myelin glycoproteins, degrading enzymes, microbial ligandsAstrocytesIschemia[>>140<<, 141]PerivascularMeningealChoroid plexus macrophages
n2:mentions
n3:15538754
Subject Item
_:vb27794922
rdf:type
n2:Context
rdf:value
disease[138, 139]FibroblastsEpithelial cellsDendritic cellsMannose receptorsSoluble immune components, cell debris, cytotoxic substances, myelin glycoproteins, degrading enzymes, microbial ligandsAstrocytesIschemia[140, >>141<<]PerivascularMeningealChoroid plexus macrophages
n2:mentions
n3:22459039
Subject Item
_:vb27794923
rdf:type
n2:Context
rdf:value
TLR1–9, which belong to interleukin (IL)-1R super-family, expressed exclusively on antigen presenting cells including microglia [>>21<<], macrophages, antigen presenting dendritic cells, and cerebral parenchyma cells which contain neurons, oligodendrites, and astrocytes.
n2:mentions
n3:23621371
Subject Item
_:vb27794924
rdf:type
n2:Context
rdf:value
TLRs not only trigger the recognition of pathogen-associated molecular patterns, such as LPS or viral nucleotides, but also recognize danger-associated molecular patterns, such as deposited amyloid β (Aβ) fibril and α-synuclein [>>22<<, 23]. TLRs are also implicated in a variety of cerebral disorders, including bacterial or viral infections; neurodegenerative disorders such as AD; inflammatory demyelinating disorders such as MS; spinal cord injury (SCI); and in
n2:mentions
n3:18809468
Subject Item
_:vb27794925
rdf:type
n2:Context
rdf:value
TLRs not only trigger the recognition of pathogen-associated molecular patterns, such as LPS or viral nucleotides, but also recognize danger-associated molecular patterns, such as deposited amyloid β (Aβ) fibril and α-synuclein [22, >>23<<]. TLRs are also implicated in a variety of cerebral disorders, including bacterial or viral infections; neurodegenerative disorders such as AD; inflammatory demyelinating disorders such as MS; spinal cord injury (SCI); and in development
n2:mentions
n3:21745188
Subject Item
_:vb27794926
rdf:type
n2:Context
rdf:value
bacterial or viral infections; neurodegenerative disorders such as AD; inflammatory demyelinating disorders such as MS; spinal cord injury (SCI); and in development or physiological processes such as neurogenesis, learning, and memory [>>22<<–25]. TLRs and TLR-dependent signaling pathways are involved in antibacterial immunity and restricting viral infection in CNS infection.
n2:mentions
n3:18809468 n3:9496822 n3:12615045 n3:21745188
Subject Item
_:vb27794927
rdf:type
n2:Context
rdf:value
Of note, TLR2 and TLR4 mediate brain injury and subsequent inflammation after ischemic stroke [>>25<<–28]. TLR4-, TLR2-, and TLR9-dependent signaling pathways are involved in mediating microglial phagocytosis of neurotoxic Aβ deposit in AD brain and exert a protective role in nerve regeneration [28–30]. It has been reported that TLRs
n2:mentions
n3:18309167 n3:17854911 n3:17548055 n3:12615045
Subject Item
_:vb27794928
rdf:type
n2:Context
rdf:value
TLR4-, TLR2-, and TLR9-dependent signaling pathways are involved in mediating microglial phagocytosis of neurotoxic Aβ deposit in AD brain and exert a protective role in nerve regeneration [>>28<<–30]. It has been reported that TLRs regulate phagocytosis through myeloid differentiation factor 88(MyD88)-dependent and MyD88-independent signaling pathways. The MyD88-dependent pathway is triggered by TLRs through activation of IL-1
n2:mentions
n3:18309167 n3:20552234 n3:16984903
Subject Item
_:vb27794929
rdf:type
n2:Context
rdf:value
The MyD88-dependent pathway is triggered by TLRs through activation of IL-1 receptor-associated kinase (IRAK)-4 and p38, resulting in up-regulation of scavenger receptors [>>31<<]. On the other hand, TLRs also regulate phagocytosis by MyD88-independent actin-Cdc42/Rac pathway [32].
n2:mentions
n3:14699082
Subject Item
_:vb27794930
rdf:type
n2:Context
rdf:value
On the other hand, TLRs also regulate phagocytosis by MyD88-independent actin-Cdc42/Rac pathway [>>32<<].
n2:mentions
n3:18542102
Subject Item
_:vb27794931
rdf:type
n2:Context
rdf:value
TREM-2 is a kind of pattern receptor specific for polyanionic and locates mainly on the cell surface of osteoclasts in bones and in microglia of the CNS [>>8<<, 33]. In addition to up-regulating the synthesis of chemokines and mediating protective phagocytosis of apoptotic cell debris, activation of TREM-2 receptors suppresses secretion of pro-inflammatory factors such as cytokines and ROS [8,
n2:mentions
n3:19409897
Subject Item
_:vb27794932
rdf:type
n2:Context
rdf:value
TREM-2 is a kind of pattern receptor specific for polyanionic and locates mainly on the cell surface of osteoclasts in bones and in microglia of the CNS [8, >>33<<]. In addition to up-regulating the synthesis of chemokines and mediating protective phagocytosis of apoptotic cell debris, activation of TREM-2 receptors suppresses secretion of pro-inflammatory factors such as cytokines and ROS [8, 33].
n2:mentions
n3:17110943
Subject Item
_:vb27794933
rdf:type
n2:Context
rdf:value
In addition to up-regulating the synthesis of chemokines and mediating protective phagocytosis of apoptotic cell debris, activation of TREM-2 receptors suppresses secretion of pro-inflammatory factors such as cytokines and ROS [>>8<<, 33]. Clinical observation showed that administration of specific agonist or antibody of TREM during the effector phase of MS led to a more severe immune response and resulted in more extensive demyelination [34]. TREM-2 on microglia via
n2:mentions
n3:19409897
Subject Item
_:vb27794934
rdf:type
n2:Context
rdf:value
In addition to up-regulating the synthesis of chemokines and mediating protective phagocytosis of apoptotic cell debris, activation of TREM-2 receptors suppresses secretion of pro-inflammatory factors such as cytokines and ROS [8, >>33<<]. Clinical observation showed that administration of specific agonist or antibody of TREM during the effector phase of MS led to a more severe immune response and resulted in more extensive demyelination [34]. TREM-2 on microglia via
n2:mentions
n3:17110943
Subject Item
_:vb27794935
rdf:type
n2:Context
rdf:value
Clinical observation showed that administration of specific agonist or antibody of TREM during the effector phase of MS led to a more severe immune response and resulted in more extensive demyelination [>>34<<]. TREM-2 on microglia via binding with DNAX-activation protein 12 (DAP12), an ITAM-containing adaptor protein, triggers the reorganization of F-actin and phosphorylation of ERK/MAPK, mediating the clearance of apoptotic neurons [34, 35].
n2:mentions
n3:17407101
Subject Item
_:vb27794936
rdf:type
n2:Context
rdf:value
TREM-2 on microglia via binding with DNAX-activation protein 12 (DAP12), an ITAM-containing adaptor protein, triggers the reorganization of F-actin and phosphorylation of ERK/MAPK, mediating the clearance of apoptotic neurons [>>34<<, 35]. Nasu–Hakola disease, a systemic bone cystic disorder with progressive presenile dementia followed by extensive sclerosis in the front-temporal lobe and the basal ganglia, occurs due to genetic mutation of TREM-2 and DAP12 resulting
n2:mentions
n3:17407101
Subject Item
_:vb27794937
rdf:type
n2:Context
rdf:value
TREM-2 on microglia via binding with DNAX-activation protein 12 (DAP12), an ITAM-containing adaptor protein, triggers the reorganization of F-actin and phosphorylation of ERK/MAPK, mediating the clearance of apoptotic neurons [34, >>35<<]. Nasu–Hakola disease, a systemic bone cystic disorder with progressive presenile dementia followed by extensive sclerosis in the front-temporal lobe and the basal ganglia, occurs due to genetic mutation of TREM-2 and DAP12 resulting in
n2:mentions
n3:15728241
Subject Item
_:vb27794938
rdf:type
n2:Context
rdf:value
disorder with progressive presenile dementia followed by extensive sclerosis in the front-temporal lobe and the basal ganglia, occurs due to genetic mutation of TREM-2 and DAP12 resulting in aberrant TREM-2/DAP12 signaling pathway [>>36<<].
n2:mentions
n3:21981270
Subject Item
_:vb27794939
rdf:type
n2:Context
rdf:value
The study of P2Y6 receptor has gained increasing attention during the past several years since the elegant demonstration that P2Y6 receptor triggers the UDP-evoked microglial phagocytosis [>>37<<]. In other words, UDP, which is released from injured neurons after trauma or ischemia, acts as “eat me” signal and meditates the P2Y6-dependent phagocytosis. P2Y6, when combined with UDP, activates phospholipase C (PLC) which in turn
n2:mentions
n3:17410128
Subject Item
_:vb27794940
rdf:type
n2:Context
rdf:value
P2Y6, when combined with UDP, activates phospholipase C (PLC) which in turn causes the synthesis of inositol 1,4,5-trisphophate (InsP3) and triggers the booted release of Ca2+ from InsP3-receptor-sensitive stores [>>37<<]. In addition to triggering the intracellular Ca2+ over-loading, P2Y6-receptor-dependent signaling pathway also triggers actin cytoskeleton polarization to shape filopodia-like protrusions, thus facilitates the engulfment of cell debris
n2:mentions
n3:17410128
Subject Item
_:vb27794941
rdf:type
n2:Context
rdf:value
In addition to triggering the intracellular Ca2+ over-loading, P2Y6-receptor-dependent signaling pathway also triggers actin cytoskeleton polarization to shape filopodia-like protrusions, thus facilitates the engulfment of cell debris [>>37<<].
n2:mentions
n3:17410128
Subject Item
_:vb27794942
rdf:type
n6:Section
dc:title
microglial phagocytosis in cns diseases
n6:contains
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Subject Item
_:vb27794943
rdf:type
n2:Context
rdf:value
Activated microglia, reactive astrocytes, and profound neuronal loss are also evident [>>38<<]. Human studies disclosed that the accumulation of Aβ deposition in the brain correlated well with cognitive impairment and neuronal loss [39]. Microglial cells play a crucial role in removing Aβ in different ways. Using 3D reconstruction
n2:mentions
n3:1785042
Subject Item
_:vb27794944
rdf:type
n2:Context
rdf:value
Human studies disclosed that the accumulation of Aβ deposition in the brain correlated well with cognitive impairment and neuronal loss [>>39<<]. Microglial cells play a crucial role in removing Aβ in different ways. Using 3D reconstruction of microglia and amyloid in an animal model of AD, Stalder et al. demonstrated that clusters of activated microglia contained lysosomes or
n2:mentions
n3:18393795
Subject Item
_:vb27794945
rdf:type
n2:Context
rdf:value
Using 3D reconstruction of microglia and amyloid in an animal model of AD, Stalder et al. demonstrated that clusters of activated microglia contained lysosomes or vacuoles in close vicinity of the dense core plaques [>>40<<]. An in vitro study of pulse-chase experiments with Cy3-labeledα2-macroglobulin (α2M) and Cy3-labeled Aβ microaggregates in the cultured microglia showed that rapid uptake of both α2M and Aβ microaggregates took place within 15 min, and
n2:mentions
n3:11378249
Subject Item
_:vb27794946
rdf:type
n2:Context
rdf:value
Interestingly, microglial cells became engorged with undigested Aβ after continuous incubation with Aβ aggregation for 4 days, suggesting a slow rate of degradation of the fibrils [>>41<<]. Bamberger et al. reported the identification of the multicomponent receptor complex of fibrillar Aβ (fAβ) on microglial cell surface [42]. The principle constituents of the complex are CD36, CD47 (also termed integrin-associated
n2:mentions
n3:9361021
Subject Item
_:vb27794947
rdf:type
n2:Context
rdf:value
Bamberger et al. reported the identification of the multicomponent receptor complex of fibrillar Aβ (fAβ) on microglial cell surface [>>42<<]. The principle constituents of the complex are CD36, CD47 (also termed integrin-associated protein), and the α6β1-integrin [43]. This receptor complex mediates the adhesion of Aβ fibrils (fAβ) to microglia and elicits phagocytosis. The
n2:mentions
n3:12684452
Subject Item
_:vb27794948
rdf:type
n2:Context
rdf:value
The principle constituents of the complex are CD36, CD47 (also termed integrin-associated protein), and the α6β1-integrin [>>43<<]. This receptor complex mediates the adhesion of Aβ fibrils (fAβ) to microglia and elicits phagocytosis. The bond of fAβ to the ensemble of receptors leads to activation of tyrosine kinase-mediated signal transduction cascades, which then
n2:mentions
n3:15525768
Subject Item
_:vb27794949
rdf:type
n2:Context
rdf:value
The bond of fAβ to the ensemble of receptors leads to activation of tyrosine kinase-mediated signal transduction cascades, which then results in a respiratory burst and production of IL-1β [>>42<<]. Koenigsknecht and Landreth provided data arguing that the cell surface receptor complex-mediated engagement of fAβ was driven principally by a novel β1-integrin-dependent mechanism, but not by classical phagocytic mechanisms mediated
n2:mentions
n3:12684452
Subject Item
_:vb27794950
rdf:type
n2:Context
rdf:value
the cell surface receptor complex-mediated engagement of fAβ was driven principally by a novel β1-integrin-dependent mechanism, but not by classical phagocytic mechanisms mediated either by Ig receptors or the complement receptor 3 [>>43<<]. Mo/Hu APPswe PS1dE9 mice are capable of producing numerous Aβ deposits in the brain.
n2:mentions
n3:15525768
Subject Item
_:vb27794951
rdf:type
n2:Context
rdf:value
animal models exhibited an increase of cerebral Aβ load, which suggested that TLRs, particularly TLR-2 and TLR-4, were involved in the phagocytosis of Aβ deposit in brain parenchyma and thus exerted a protective role in AD patients [>>29<<]. FcR-mediated phagocytosis and complement activation also play a critical role in removal of plaques from the AD brain [30].
n2:mentions
n3:16984903
Subject Item
_:vb27794952
rdf:type
n2:Context
rdf:value
FcR-mediated phagocytosis and complement activation also play a critical role in removal of plaques from the AD brain [>>30<<]. Additionally, monocyte chemotactic protein-1 (MCP-1/CCL2), coupled with its binding receptor, CC-chemokine receptor 2, was crucial in neuroinflammatory response that affected disease process in a mouse model of AD [44–46].
n2:mentions
n3:20552234
Subject Item
_:vb27794953
rdf:type
n2:Context
rdf:value
Additionally, monocyte chemotactic protein-1 (MCP-1/CCL2), coupled with its binding receptor, CC-chemokine receptor 2, was crucial in neuroinflammatory response that affected disease process in a mouse model of AD [>>44<<–46]. CCL2-deficient AD mice (APP/PS1 mice) showed decreased microglial phagocytosis for both monomeric and oligomeric Aβ42 and accelerated Aβ deposits and oligomers [46]. Interestingly, transgenic overexpression of CCL-2 in APP/CCL2 mice
n2:mentions
n3:23040664 n3:19593388 n3:23771498
Subject Item
_:vb27794954
rdf:type
n2:Context
rdf:value
CCL2-deficient AD mice (APP/PS1 mice) showed decreased microglial phagocytosis for both monomeric and oligomeric Aβ42 and accelerated Aβ deposits and oligomers [>>46<<]. Interestingly, transgenic overexpression of CCL-2 in APP/CCL2 mice dramatically facilitated Aβ uptake and subsequent intracellular Aβ oligomerization and resulted in progression of neurocognitive decline [45]. The exact role of CCL-2 in
n2:mentions
n3:23040664
Subject Item
_:vb27794955
rdf:type
n2:Context
rdf:value
Interestingly, transgenic overexpression of CCL-2 in APP/CCL2 mice dramatically facilitated Aβ uptake and subsequent intracellular Aβ oligomerization and resulted in progression of neurocognitive decline [>>45<<]. The exact role of CCL-2 in AD remains further study. Koenigsknecht-Talboo and Landreth have studied that the pro-inflammatory environment of the AD brain impaired the microglial capacity of removal of Aβ, whereas anti-inflammatory
n2:mentions
n3:19593388
Subject Item
_:vb27794956
rdf:type
n2:Context
rdf:value
Koenigsknecht-Talboo and Landreth have studied that the pro-inflammatory environment of the AD brain impaired the microglial capacity of removal of Aβ, whereas anti-inflammatory factors enhanced Aβ clearance [>>47<<]. Microglia treated with pro-inflammatory cytokines such as LPS, IL-1β, TNF-α, IFN-γ, MCP-1, and CD40L suppressed fAβ-stimulated microglial phagocytic activity in vitro [47]. This effect was even significant during activation of the CR3
n2:mentions
n3:16148231
Subject Item
_:vb27794957
rdf:type
n2:Context
rdf:value
Microglia treated with pro-inflammatory cytokines such as LPS, IL-1β, TNF-α, IFN-γ, MCP-1, and CD40L suppressed fAβ-stimulated microglial phagocytic activity in vitro [>>47<<]. This effect was even significant during activation of the CR3 or fAβ receptor complex, but did not affect IgG- or FcR-mediated phagocytosis [47]. On the other hand, when BV2 cells were incubated with anti-inflammatory cytokines in a
n2:mentions
n3:16148231
Subject Item
_:vb27794958
rdf:type
n2:Context
rdf:value
This effect was even significant during activation of the CR3 or fAβ receptor complex, but did not affect IgG- or FcR-mediated phagocytosis [>>47<<]. On the other hand, when BV2 cells were incubated with anti-inflammatory cytokines in a pro-inflammatory milieu, these phagocytes exhibited a stronger competence to uptake fibrillar Aβ [47]. Anti-inflammatory cytokines, such as IL-4,
n2:mentions
n3:16148231
Subject Item
_:vb27794959
rdf:type
n2:Context
rdf:value
On the other hand, when BV2 cells were incubated with anti-inflammatory cytokines in a pro-inflammatory milieu, these phagocytes exhibited a stronger competence to uptake fibrillar Aβ [>>47<<]. Anti-inflammatory cytokines, such as IL-4, IL-10, cyclooxygenase (COX) inhibitors, ibuprofen, or an E prostanoid receptor antagonist, blocked NFκB-dependent stimulation of COX-2 expression and prostaglandin E2 (PGE2) production or its
n2:mentions
n3:16148231
Subject Item
_:vb27794960
rdf:type
n2:Context
rdf:value
stimulation of COX-2 expression and prostaglandin E2 (PGE2) production or its cascade pathways to eliminate the inhibitory activity of pro-inflammatory cytokines and consequently restored fAβ-stimulated phagocytic response [>>42<<, 43, 47, 48]. These observations are consistent with previous demonstration that deletion of PGE2 EP2 receptor in animal model of familial AD resulted in a marked reduction of Aβ plaque burden and enhanced phagocytosis [49].
n2:mentions
n3:12684452
Subject Item
_:vb27794961
rdf:type
n2:Context
rdf:value
stimulation of COX-2 expression and prostaglandin E2 (PGE2) production or its cascade pathways to eliminate the inhibitory activity of pro-inflammatory cytokines and consequently restored fAβ-stimulated phagocytic response [42, >>43<<, 47, 48]. These observations are consistent with previous demonstration that deletion of PGE2 EP2 receptor in animal model of familial AD resulted in a marked reduction of Aβ plaque burden and enhanced phagocytosis [49].
n2:mentions
n3:15525768
Subject Item
_:vb27794962
rdf:type
n2:Context
rdf:value
stimulation of COX-2 expression and prostaglandin E2 (PGE2) production or its cascade pathways to eliminate the inhibitory activity of pro-inflammatory cytokines and consequently restored fAβ-stimulated phagocytic response [42, 43, >>47<<, 48]. These observations are consistent with previous demonstration that deletion of PGE2 EP2 receptor in animal model of familial AD resulted in a marked reduction of Aβ plaque burden and enhanced phagocytosis [49].
n2:mentions
n3:16148231
Subject Item
_:vb27794963
rdf:type
n2:Context
rdf:value
stimulation of COX-2 expression and prostaglandin E2 (PGE2) production or its cascade pathways to eliminate the inhibitory activity of pro-inflammatory cytokines and consequently restored fAβ-stimulated phagocytic response [42, 43, 47, >>48<<]. These observations are consistent with previous demonstration that deletion of PGE2 EP2 receptor in animal model of familial AD resulted in a marked reduction of Aβ plaque burden and enhanced phagocytosis [49].
n2:mentions
n3:14764680
Subject Item
_:vb27794964
rdf:type
n2:Context
rdf:value
These observations are consistent with previous demonstration that deletion of PGE2 EP2 receptor in animal model of familial AD resulted in a marked reduction of Aβ plaque burden and enhanced phagocytosis [>>49<<].
n2:mentions
n3:16267225
Subject Item
_:vb27794965
rdf:type
n2:Context
rdf:value
Although microglia exhibit “activated” phenotype, they are presumably unable to efficiently uptake Aβ plaque to prevent the neurodegenerative progression of AD patients [>>42<<]. Treatment with antibodies against Aβ peptide to PDAPP transgenic mouse model of AD dramatically reduced Aβ deposit by facilitating clearance of preexisting amyloid rather than by simply preventing new plaques formation [50].
n2:mentions
n3:12684452
Subject Item
_:vb27794966
rdf:type
n2:Context
rdf:value
Treatment with antibodies against Aβ peptide to PDAPP transgenic mouse model of AD dramatically reduced Aβ deposit by facilitating clearance of preexisting amyloid rather than by simply preventing new plaques formation [>>50<<]. Recent studies showed that treatment with anti-Aβ antibodies may be effective in reducing plaque burden and reversing memory deficits in mouse model for AD [51, 52]. Therefore, modulating phagocytosis and degradation of fAβ by microglia
n2:mentions
n3:10932230
Subject Item
_:vb27794967
rdf:type
n2:Context
rdf:value
Recent studies showed that treatment with anti-Aβ antibodies may be effective in reducing plaque burden and reversing memory deficits in mouse model for AD [>>51<<, 52]. Therefore, modulating phagocytosis and degradation of fAβ by microglia might be a potential treatment of AD.
n2:mentions
n3:11438712
Subject Item
_:vb27794968
rdf:type
n2:Context
rdf:value
Recent studies showed that treatment with anti-Aβ antibodies may be effective in reducing plaque burden and reversing memory deficits in mouse model for AD [51, >>52<<]. Therefore, modulating phagocytosis and degradation of fAβ by microglia might be a potential treatment of AD.
n2:mentions
n3:12736345
Subject Item
_:vb27794969
rdf:type
n2:Context
rdf:value
SCI occurs from a primary mechanical insult on the spinal cord, resulting in damage of neurons and axons [>>53<<], followed by a second-wave injury.
n2:mentions
n3:8787776
Subject Item
_:vb27794970
rdf:type
n2:Context
rdf:value
Microglia, as the principal immune effectors in the brain, undergo a conversion into a reactive pro-inflammatory phenotype in neurotrauma rapidly [>>54<<]. ED1-positive microglia began to be detected at 6 h after SCI and mostly located close to the lesion epicenter [55]. Within 48 h post-injury, the ED-1 positive microglia showed the tendency of a higher density and a broader
n2:mentions
n3:21400005
Subject Item
_:vb27794971
rdf:type
n2:Context
rdf:value
ED1-positive microglia began to be detected at 6 h after SCI and mostly located close to the lesion epicenter [>>55<<]. Within 48 h post-injury, the ED-1 positive microglia showed the tendency of a higher density and a broader macrophages/microglia infiltrating extension [55]. It is striking that a higher density of macrophages/microglia in the gray
n2:mentions
n3:9582256
Subject Item
_:vb27794972
rdf:type
n2:Context
rdf:value
Within 48 h post-injury, the ED-1 positive microglia showed the tendency of a higher density and a broader macrophages/microglia infiltrating extension [>>55<<]. It is striking that a higher density of macrophages/microglia in the gray matter than white matter continued to be observed [55]. Since activated microglia and infiltrated peripheral macrophages exhibit the similar morphology, gene
n2:mentions
n3:9582256
Subject Item
_:vb27794973
rdf:type
n2:Context
rdf:value
It is striking that a higher density of macrophages/microglia in the gray matter than white matter continued to be observed [>>55<<]. Since activated microglia and infiltrated peripheral macrophages exhibit the similar morphology, gene expression, as well as surface and endocellular markers, there is still no discriminating cellular markers to distinguish these two
n2:mentions
n3:9582256
Subject Item
_:vb27794974
rdf:type
n2:Context
rdf:value
Accumulating evidence has shown that microglia play a pivotal role in the process of spinal cord regeneration and degeneration during the so-called secondary injury [>>11<<]. Microglia, when exposed to myelin in vitro, rapidly transformed from ramified to activated amoeboid morphology.
n2:mentions
n3:20880501
Subject Item
_:vb27794975
rdf:type
n2:Context
rdf:value
In a dog model for SCI, a significant myelinophagia occurred 5 days after trauma, which was concomitant to the phagocytic activation of microglia [>>56<<]. An enhanced phagocytic capacity of single microglial cell was observed, particularly in the early 5 days, but the number of phagocytes did not change [56].
n2:mentions
n3:21599492
Subject Item
_:vb27794976
rdf:type
n2:Context
rdf:value
An enhanced phagocytic capacity of single microglial cell was observed, particularly in the early 5 days, but the number of phagocytes did not change [>>56<<]. In this study, the capacity of microglial phagocytosis was measured by flow cytometric assay using FITC-labeled Staphylococcus aureus. The bacteria were added into microglial cell suspension to determine the percentage of microglia with
n2:mentions
n3:21599492
Subject Item
_:vb27794977
rdf:type
n2:Context
rdf:value
However, in the later stage, number of microglia with phagocytic phenotype increased, accompanied by less activity of phagocytosis of individual cell [>>56<<]. The rapid clearance of degenerated myelin is beneficial to trigger efficient remyelination.
n2:mentions
n3:21599492
Subject Item
_:vb27794978
rdf:type
n2:Context
rdf:value
The early studies by Cullheim and Thams elegantly demonstrated that major histocompatibility complex (MHC) class I molecules and MHC class I receptors played a key role in synaptic plasticity and nerve-regeneration after axonomy [>>57<<]. Synaptic stripping preferred to remove excitotoxic glutamatergic rather than the inhibitory glycinergic and GABAergic nerve terminals, suggesting a beneficial effect for the repair. Functional MHC class I took part in normal “stripping”
n2:mentions
n3:17509690
Subject Item
_:vb27794979
rdf:type
n2:Context
rdf:value
a subunit of MHC class I and transporter associated with antigen processing 1 knockdown or knockout mice, displayed remarkable elimination of synapses, resulting in less synaptic terminals remaining on the surface of affected neurons [>>57<<]. This observation was supported by a recent study by Sabha and colleagues showing a robust up-regulation of MHC I class after axonomy in different mice strains [58].
n2:mentions
n3:17509690
Subject Item
_:vb27794980
rdf:type
n2:Context
rdf:value
This observation was supported by a recent study by Sabha and colleagues showing a robust up-regulation of MHC I class after axonomy in different mice strains [>>58<<]. C57BL/6J mice with a low level of MHC I expression showed poor axon regeneration and slow synaptic stripping from motor neuron surface following peripheral nerve axonomy [58]. Additionally, A/J mice after axonomy exhibited significant
n2:mentions
n3:18000810
Subject Item
_:vb27794981
rdf:type
n2:Context
rdf:value
C57BL/6J mice with a low level of MHC I expression showed poor axon regeneration and slow synaptic stripping from motor neuron surface following peripheral nerve axonomy [>>58<<]. Additionally, A/J mice after axonomy exhibited significant elevation of MHC I expression and stronger regenerative potential, accompanied with more intense of synaptic elimination [58]. Zanon and colleagues indicated that IFN-β
n2:mentions
n3:18000810
Subject Item
_:vb27794982
rdf:type
n2:Context
rdf:value
Additionally, A/J mice after axonomy exhibited significant elevation of MHC I expression and stronger regenerative potential, accompanied with more intense of synaptic elimination [>>58<<]. Zanon and colleagues indicated that IFN-β treatment notably increased MHC class I expression after sciatic nerve crush in mice [59].
n2:mentions
n3:18000810
Subject Item
_:vb27794983
rdf:type
n2:Context
rdf:value
Zanon and colleagues indicated that IFN-β treatment notably increased MHC class I expression after sciatic nerve crush in mice [>>59<<].
n2:mentions
n3:20831746
Subject Item
_:vb27794984
rdf:type
n2:Context
rdf:value
that CD47 (also known as integrin-associated protein), expressed on myelin, when reacting to immune inhibitory receptor signal regulatory protein-α (SIRP-α) on microglia, notably down-regulated myelin phagocytosis by microglia in vitro [>>60<<]. This finding suggested that CD47 on one hand exerts a neuroprotective function by protecting normal intact myelin from activated phagocytes, while on the other hand impedes normal phagocytosis therefore is unfavorable to the repair of
n2:mentions
n3:21401967
Subject Item
_:vb27794985
rdf:type
n2:Context
rdf:value
Previous experiments have demonstrated that complement receptor-3 (CR3/MAC-1) signaling pathway was involved in the clearance of degenerated myelin [>>61<<]. CR3/MAC-1, as a member of integrin superfamily, is composed by αM and β2 subunit [62] and mediates myelin phagocytosis via binding to both complement (iC3b) and noncomplement ligand (e.g., fibrinogen and I-CAM) [61]. A study by
n2:mentions
n3:14500997
Subject Item
_:vb27794986
rdf:type
n2:Context
rdf:value
CR3/MAC-1, as a member of integrin superfamily, is composed by αM and β2 subunit [>>62<<] and mediates myelin phagocytosis via binding to both complement (iC3b) and noncomplement ligand (e.g., fibrinogen and I-CAM) [61].
n2:mentions
n3:9728397
Subject Item
_:vb27794987
rdf:type
n2:Context
rdf:value
CR3/MAC-1, as a member of integrin superfamily, is composed by αM and β2 subunit [62] and mediates myelin phagocytosis via binding to both complement (iC3b) and noncomplement ligand (e.g., fibrinogen and I-CAM) [>>61<<]. A study by Rotshenker and colleagues demonstrated that CR3/MAC-1 activated guanine nucleotide exchange factors that facilitated the conversion of inactive K-Ras-GDP to active K-Ras-GTP, which then led to activation of PI3K and myelin
n2:mentions
n3:14500997
Subject Item
_:vb27794988
rdf:type
n2:Context
rdf:value
Rotshenker and colleagues demonstrated that CR3/MAC-1 activated guanine nucleotide exchange factors that facilitated the conversion of inactive K-Ras-GDP to active K-Ras-GTP, which then led to activation of PI3K and myelin phagocytosis [>>63<<]. Treating microglia with TNF-α suppressed myelin phagocytosis mediated by CR3/MAC-1 [64].
n2:mentions
n3:18615637
Subject Item
_:vb27794989
rdf:type
n2:Context
rdf:value
Treating microglia with TNF-α suppressed myelin phagocytosis mediated by CR3/MAC-1 [>>64<<]. Scavenger receptor AI/II (SRAI/II) also participates in myelin clearance after trauma. However, the relative potential contribution of CR3/MAC-1 to myelin phagocytosis is two- or three-folds more than that of SRAI/II [65]. Microglia
n2:mentions
n3:1349613
Subject Item
_:vb27794990
rdf:type
n2:Context
rdf:value
However, the relative potential contribution of CR3/MAC-1 to myelin phagocytosis is two- or three-folds more than that of SRAI/II [>>65<<]. Microglia immunophenotypical characterization in dogs with SCI revealed a remarkable upregulation of mediators for phagocytosis, including ICAM-I, CD14, CD44, and CD45, and the increasing of expression intensity of these surface
n2:mentions
n3:12609490
Subject Item
_:vb27794991
rdf:type
n2:Context
rdf:value
SCI revealed a remarkable upregulation of mediators for phagocytosis, including ICAM-I, CD14, CD44, and CD45, and the increasing of expression intensity of these surface molecules significantly enhanced the removal of tissue debris [>>56<<].
n2:mentions
n3:21599492
Subject Item
_:vb27794992
rdf:type
n2:Context
rdf:value
as Nogo-A, myelin-associated glycoprotein, oligodendrocytes myelin glycoprotein, the transmembrane semaphoring 4D (Sema4D/CD100), and ephrinB3, translocate to cell surface on injured myelin and act as inhibitors of axonal regeneration [>>66<<]. Therefore, efficient microglial phagocytosis of damaged myelin and cell debris is beneficial for the survival of injured neurons and myelin regeneration in acute SCI and TBI [56, 67].
n2:mentions
n3:16858390
Subject Item
_:vb27794993
rdf:type
n2:Context
rdf:value
Therefore, efficient microglial phagocytosis of damaged myelin and cell debris is beneficial for the survival of injured neurons and myelin regeneration in acute SCI and TBI [>>56<<, 67]. The enhanced microglial phagocytosis of myelin debris was demonstrated dramatically to decrease dead cells and myelin debris and result in prominent functional recovery [61].
n2:mentions
n3:21599492
Subject Item
_:vb27794994
rdf:type
n2:Context
rdf:value
Therefore, efficient microglial phagocytosis of damaged myelin and cell debris is beneficial for the survival of injured neurons and myelin regeneration in acute SCI and TBI [56, >>67<<]. The enhanced microglial phagocytosis of myelin debris was demonstrated dramatically to decrease dead cells and myelin debris and result in prominent functional recovery [61].
n2:mentions
n3:24112298
Subject Item
_:vb27794995
rdf:type
n2:Context
rdf:value
The enhanced microglial phagocytosis of myelin debris was demonstrated dramatically to decrease dead cells and myelin debris and result in prominent functional recovery [>>61<<].
n2:mentions
n3:14500997
Subject Item
_:vb27794996
rdf:type
n2:Context
rdf:value
Rapid infiltration of polymorphonuclear neutrophils (PMNs) and peripheral monocytes/macrophages and abundant activation of resident microglia are observed in the injured brain post-ischemia lesion [>>68<<, 69]. In an in vivo study, Schilling et al. demonstrated that both resident microglia and hematogenous macrophages made contributions to debris clearance post-cerebral infarction, while microglia played a more major role than did
n2:mentions
n3:10441299
Subject Item
_:vb27794997
rdf:type
n2:Context
rdf:value
Rapid infiltration of polymorphonuclear neutrophils (PMNs) and peripheral monocytes/macrophages and abundant activation of resident microglia are observed in the injured brain post-ischemia lesion [68, >>69<<]. In an in vivo study, Schilling et al. demonstrated that both resident microglia and hematogenous macrophages made contributions to debris clearance post-cerebral infarction, while microglia played a more major role than did macrophages
n2:mentions
n3:18524901
Subject Item
_:vb27794998
rdf:type
n2:Context
rdf:value
In an in vivo study, Schilling et al. demonstrated that both resident microglia and hematogenous macrophages made contributions to debris clearance post-cerebral infarction, while microglia played a more major role than did macrophages [>>70<<]. Activated microglia were observed to rapidly migrated into the infarction area and elicited phagocytic response at day 1 after ischemia [71, 72], but no peripheral infiltration was seen [70].
n2:mentions
n3:16153641
Subject Item
_:vb27794999
rdf:type
n2:Context
rdf:value
Activated microglia were observed to rapidly migrated into the infarction area and elicited phagocytic response at day 1 after ischemia [>>71<<, 72], but no peripheral infiltration was seen [70].
n2:mentions
n3:8896826
Subject Item
_:vb27795000
rdf:type
n2:Context
rdf:value
Activated microglia were observed to rapidly migrated into the infarction area and elicited phagocytic response at day 1 after ischemia [71, >>72<<], but no peripheral infiltration was seen [70].
n2:mentions
n3:8432904
Subject Item
_:vb27795001
rdf:type
n2:Context
rdf:value
Activated microglia were observed to rapidly migrated into the infarction area and elicited phagocytic response at day 1 after ischemia [71, 72], but no peripheral infiltration was seen [>>70<<]. The total number of activated microglia showed an increased tendency in the following several days and reached maximum at day 10 after transient focal cerebral ischemia [70], whereas blood-borne macrophages began to occur in the damaged
n2:mentions
n3:16153641
Subject Item
_:vb27795002
rdf:type
n2:Context
rdf:value
The total number of activated microglia showed an increased tendency in the following several days and reached maximum at day 10 after transient focal cerebral ischemia [>>70<<], whereas blood-borne macrophages began to occur in the damaged lesion at day 4, increased to the peak number in the following 3 days, and began to decrease until 2 weeks after ischemic insult [70].
n2:mentions
n3:16153641
Subject Item
_:vb27795003
rdf:type
n2:Context
rdf:value
transient focal cerebral ischemia [70], whereas blood-borne macrophages began to occur in the damaged lesion at day 4, increased to the peak number in the following 3 days, and began to decrease until 2 weeks after ischemic insult [>>70<<]. Strikingly, phagocytic microglia only accounted for one quarter of the total activated microglia.
n2:mentions
n3:16153641
Subject Item
_:vb27795004
rdf:type
n2:Context
rdf:value
This phenotype of microglia rapidly had their maximum number as early as day 1 and stayed at the same level within the following days until the hematogenous macrophages infiltrated [>>70<<]. These findings lead to the hypothesis that participation of microglia in the debris clearance takes place in the early stage while the assistance from blood-borne macrophages infiltration in the infarction zone occurs later.
n2:mentions
n3:16153641
Subject Item
_:vb27795005
rdf:type
n2:Context
rdf:value
In vivo study showed that PMN rapidly infiltrated and accumulated in ischemic-injured brain as early as day 1 after cerebral ischemia [>>69<<, 73]. Application of PMNs onto post-oxygen–glucose deprivation organotypic hippocampal slice cultures (OGD-OHCs) led to a remarkable exacerbation of neuronal damage, characterized by severe loss of axons and dendrites, as well as the
n2:mentions
n3:18524901
Subject Item
_:vb27795006
rdf:type
n2:Context
rdf:value
In vivo study showed that PMN rapidly infiltrated and accumulated in ischemic-injured brain as early as day 1 after cerebral ischemia [69, >>73<<]. Application of PMNs onto post-oxygen–glucose deprivation organotypic hippocampal slice cultures (OGD-OHCs) led to a remarkable exacerbation of neuronal damage, characterized by severe loss of axons and dendrites, as well as the
n2:mentions
n3:14684829
Subject Item
_:vb27795007
rdf:type
n2:Context
rdf:value
slice cultures (OGD-OHCs) led to a remarkable exacerbation of neuronal damage, characterized by severe loss of axons and dendrites, as well as the appearance of apoptotic or necrotic neurons containing subcellular material at day 1 [>>69<<]. Interestingly, the co-application of PMNs and microglia onto the OGD-OHCs significantly reduced the PMN-induced damage to neurons, which was presumably due to direct engulfment of those viable, motile, and nonapoptotic PMNs by microglia
n2:mentions
n3:18524901
Subject Item
_:vb27795008
rdf:type
n2:Context
rdf:value
the co-application of PMNs and microglia onto the OGD-OHCs significantly reduced the PMN-induced damage to neurons, which was presumably due to direct engulfment of those viable, motile, and nonapoptotic PMNs by microglia [>>69<<]. Uptake of PMNs by microglia significantly reduced the release of pro-inflammatory mediators, such as cytokines and ROS, and was associated with the upregulation of TGF-β in microglia, both of which exerted a beneficial role in the
n2:mentions
n3:18524901
Subject Item
_:vb27795009
rdf:type
n2:Context
rdf:value
PMNs by microglia significantly reduced the release of pro-inflammatory mediators, such as cytokines and ROS, and was associated with the upregulation of TGF-β in microglia, both of which exerted a beneficial role in the injured brain [>>69<<]. The exact mechanisms and signals involved in recognition and uptake of PMN by microglia are not yet defined.
n2:mentions
n3:18524901
Subject Item
_:vb27795010
rdf:type
n2:Context
rdf:value
Furthermore, microglia also elicited phagocytic response through interaction with cell surface receptors, for example, osteopontin (OPN), an adhesive glycoprotein [>>74<<]. It has previously been accepted that OPN acts only as a chemoattractant after ischemic insult, but recently, it has been reported that OPN also takes part in the phagocytosis of the cell debris [75]. Elevated expression of OPN protein
n2:mentions
n3:21264948
Subject Item
_:vb27795011
rdf:type
n2:Context
rdf:value
It has previously been accepted that OPN acts only as a chemoattractant after ischemic insult, but recently, it has been reported that OPN also takes part in the phagocytosis of the cell debris [>>75<<]. Elevated expression of OPN protein was seen mainly along the membranes lining after ischemic stroke; thus, researchers concluded that OPN elicited phagocytic response of fragmented debris selectively [74].
n2:mentions
n3:18656563
Subject Item
_:vb27795012
rdf:type
n2:Context
rdf:value
Elevated expression of OPN protein was seen mainly along the membranes lining after ischemic stroke; thus, researchers concluded that OPN elicited phagocytic response of fragmented debris selectively [>>74<<].
n2:mentions
n3:21264948
Subject Item
_:vb27795013
rdf:type
n2:Context
rdf:value
Overexpression of extracellular α-synuclein is a well-known etiological pathology of PD [>>76<<]. Microglia treated with monomeric α-synuclein exhibited an enhanced phagocytic activity in vitro, in a both time- and dose-dependent manner [77]. In this study, microglial phagocytosis was evaluated by the activity of microglia in
n2:mentions
n3:15952880
Subject Item
_:vb27795014
rdf:type
n2:Context
rdf:value
Microglia treated with monomeric α-synuclein exhibited an enhanced phagocytic activity in vitro, in a both time- and dose-dependent manner [>>77<<]. In this study, microglial phagocytosis was evaluated by the activity of microglia in ingesting extracellular fluorescent microspheres. The exact mechanism underlying in monomeric α-synuclein induced phagocytosis by microglia is still an
n2:mentions
n3:18449945
Subject Item
_:vb27795015
rdf:type
n2:Context
rdf:value
Studies have confirmed the involvement of CR3, α6β1, and CD47, which are important components of receptor complex in clearance of Aβ [>>77<<]. In comparison, aggregated α-synuclein inhibited phagocytosis of cell debris and dead neurons not only by antagonizing monomeric-facilitated clearance but also through decreasing the basal microglial phagocytic capability [77]. It is
n2:mentions
n3:18449945
Subject Item
_:vb27795016
rdf:type
n2:Context
rdf:value
In comparison, aggregated α-synuclein inhibited phagocytosis of cell debris and dead neurons not only by antagonizing monomeric-facilitated clearance but also through decreasing the basal microglial phagocytic capability [>>77<<]. It is also reported that microglia were capable of phagocytosing and degenerating neuromelanin (NM) released from degenerated dopaminergic neurons. Microglia co-cultured with NM revealed a rapid transform from a ramified to an amoeboid
n2:mentions
n3:18449945
Subject Item
_:vb27795017
rdf:type
n2:Context
rdf:value
Microglia co-cultured with NM revealed a rapid transform from a ramified to an amoeboid morphology and were engaged in attaching to and engulfing NM particles [>>78<<]. In a 6-hydroxydopamine (6-OHDA) model of PD, phagocytic microglia (CD68 positive) were found to surround the intact tyrosine hydroxylase-positive dopaminergic substantia nigra pars compacta (SNc) neurons to remove damaged NM particles
n2:mentions
n3:19957214
Subject Item
_:vb27795018
rdf:type
n2:Context
rdf:value
A vast proportion of phagocytic microglia (CD68 positive) were seen to adhere to and engulf degenerated dopaminergic neurons and axons [>>79<<]. Using proteomic technology, Liu et al. have shown that a variety of types of membrane proteins were potentially involved in the internalization of α-synuclein [80]. Clathrin was demonstrated to play a critical role in the endocytosis of
n2:mentions
n3:19549006
Subject Item
_:vb27795019
rdf:type
n2:Context
rdf:value
Using proteomic technology, Liu et al. have shown that a variety of types of membrane proteins were potentially involved in the internalization of α-synuclein [>>80<<]. Clathrin was demonstrated to play a critical role in the endocytosis of aggregated α-synuclein, probably in a receptor-ligand sequestration-related manner [80], but the exact mechanism needs further study. Recently, TLR4 signaling
n2:mentions
n3:17676786
Subject Item
_:vb27795020
rdf:type
n2:Context
rdf:value
Clathrin was demonstrated to play a critical role in the endocytosis of aggregated α-synuclein, probably in a receptor-ligand sequestration-related manner [>>80<<], but the exact mechanism needs further study.
n2:mentions
n3:17676786
Subject Item
_:vb27795021
rdf:type
n2:Context
rdf:value
Recently, TLR4 signaling pathway is demonstrated to mediate α-synuclein phagocytosis and exert a beneficial role in deferring disease progression both in vivo and in vitro [>>81<<]. In in vivo study of transgenic murine model of α-synucleinopathies (ASP), mice overexpressed human α-synuclein (hAS) with TLR4 deficiency (AS/TLR4−/−) exhibited severer neuronal loss, motor disability, and predominant reduced phagocytic
n2:mentions
n3:21801874
Subject Item
_:vb27795022
rdf:type
n2:Context
rdf:value
with immunogold labeling for AS in the brain of transgenic mice, microglia in AS/TLR4+/+ mice showed abundant gold particles in phagocytic cytoplasmic organelles, while fewer gold particles were found in microglia in AS/TLR4−/− mice [>>81<<]. Numerous studies also displayed that C1q-mediated pathway [82] scavenger receptors [83] and MAC-1 [78] are also involved in microglial endocytosis of α-synuclein.
n2:mentions
n3:21801874
Subject Item
_:vb27795023
rdf:type
n2:Context
rdf:value
Numerous studies also displayed that C1q-mediated pathway [>>82<<] scavenger receptors [83] and MAC-1 [78] are also involved in microglial endocytosis of α-synuclein.
n2:mentions
n3:21343881
Subject Item
_:vb27795024
rdf:type
n2:Context
rdf:value
Numerous studies also displayed that C1q-mediated pathway [82] scavenger receptors [>>83<<] and MAC-1 [78] are also involved in microglial endocytosis of α-synuclein.
n2:mentions
n3:22223122
Subject Item
_:vb27795025
rdf:type
n2:Context
rdf:value
Numerous studies also displayed that C1q-mediated pathway [82] scavenger receptors [83] and MAC-1 [>>78<<] are also involved in microglial endocytosis of α-synuclein.
n2:mentions
n3:19957214
Subject Item
_:vb27795026
rdf:type
n2:Context
rdf:value
a-synuclein(A30P and A30T) in BV2 cells resulted in downregulation of phagocytosing bioparticles and a marked low lysosomal associated protein 1 expression, accompanied with elevated COX-2 and proinflammatory cytokines such as PGE2 [>>84<<].
n2:mentions
n3:18492487
Subject Item
_:vb27795027
rdf:type
n2:Context
rdf:value
Among them, microglia showed to be the most effective [>>85<<]. Whether microglial phagocytosis of α-synuclein favors or harms the process of PD is still under debate.
n2:mentions
n3:21554732
Subject Item
_:vb27795028
rdf:type
n2:Context
rdf:value
Zhang et al. argued that internalization of α-synuclein took a central role in dopaminergic neurotoxicity through activation of NADPH oxidase and subsequently oxidative stress [>>86<<]. However, as mentioned above, impaired microglial phagocytic capacity by ablation of TLR4 in ASP mouse model led to aggregation of extracellular α-synuclein and accelerated neurodegeneration. In brief, the role of microglial phagocytosis
n2:mentions
n3:15791003
Subject Item
_:vb27795029
rdf:type
n2:Context
rdf:value
Although ALS is overwhelmingly a sporadic disorder, genetic studies have established that mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene are the most well-known cause of familial ALS [>>87<<, 88]. Studies have shown that microglia has an important function in propagation of the disease process both in sporadic and familial ALS [89, 90] and in the transgenic animals overexpressing human mutant SOD1 (hmSOD1) [91]. By analysis
n2:mentions
n3:8446170
Subject Item
_:vb27795030
rdf:type
n2:Context
rdf:value
Although ALS is overwhelmingly a sporadic disorder, genetic studies have established that mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene are the most well-known cause of familial ALS [87, >>88<<]. Studies have shown that microglia has an important function in propagation of the disease process both in sporadic and familial ALS [89, 90] and in the transgenic animals overexpressing human mutant SOD1 (hmSOD1) [91]. By analysis of
n2:mentions
n3:24283690
Subject Item
_:vb27795031
rdf:type
n2:Context
rdf:value
Studies have shown that microglia has an important function in propagation of the disease process both in sporadic and familial ALS [>>89<<, 90] and in the transgenic animals overexpressing human mutant SOD1 (hmSOD1) [91].
n2:mentions
n3:1347673
Subject Item
_:vb27795032
rdf:type
n2:Context
rdf:value
Studies have shown that microglia has an important function in propagation of the disease process both in sporadic and familial ALS [89, >>90<<] and in the transgenic animals overexpressing human mutant SOD1 (hmSOD1) [91].
n2:mentions
n3:8891072
Subject Item
_:vb27795033
rdf:type
n2:Context
rdf:value
Studies have shown that microglia has an important function in propagation of the disease process both in sporadic and familial ALS [89, 90] and in the transgenic animals overexpressing human mutant SOD1 (hmSOD1) [>>91<<]. By analysis of autopsy cases of ALS, increased numbers of macrophages were observed in the regions with motor neuron loss, such as lower motor neuron XII, upper motor neuron beta cells, spinocerebellar inferior olivary nuclei and red
n2:mentions
n3:20109233
Subject Item
_:vb27795034
rdf:type
n2:Context
rdf:value
loss, such as lower motor neuron XII, upper motor neuron beta cells, spinocerebellar inferior olivary nuclei and red nuclei, somatosensory caudate nuclei and thalamus, cerebral cortex amygdaloid, and the ventral horn of the spinal cord [>>90<<]. This observation is supported by a recent experimental study which argued that activated microglia aggregated in the anterior horn of the lumbar spinal cord, particularly around impaired motor neurons [92].
n2:mentions
n3:8891072
Subject Item
_:vb27795035
rdf:type
n2:Context
rdf:value
This observation is supported by a recent experimental study which argued that activated microglia aggregated in the anterior horn of the lumbar spinal cord, particularly around impaired motor neurons [>>92<<]. This study also demonstrated that activated microglia attached to somata of motoneurons and exhibited phagocytic properties as early as presymptomatic stage [92]. Interestingly, activated microglia were visualized not only in regions
n2:mentions
n3:20648658
Subject Item
_:vb27795036
rdf:type
n2:Context
rdf:value
This study also demonstrated that activated microglia attached to somata of motoneurons and exhibited phagocytic properties as early as presymptomatic stage [>>92<<]. Interestingly, activated microglia were visualized not only in regions where there was severe motor neuron loss but also in areas of mild motor neuronal damage [90]. However, the exact role of microglia in motor neuron degeneration
n2:mentions
n3:20648658
Subject Item
_:vb27795037
rdf:type
n2:Context
rdf:value
Interestingly, activated microglia were visualized not only in regions where there was severe motor neuron loss but also in areas of mild motor neuronal damage [>>90<<]. However, the exact role of microglia in motor neuron degeneration remains unclear. In transgenic hmSOD1 (G93A) rat, it has been shown that CD11b-positive macrophages/microglia accumulated both in the ventral horn and more distally at
n2:mentions
n3:8891072
Subject Item
_:vb27795038
rdf:type
n2:Context
rdf:value
microglia may cause damage to nearby motor neurons through secretion of proinflammatory factors at the early stage of ALS, while play a neuroprotective role through phagocytosing the degenerated debris following clinical onset [>>91<<].
n2:mentions
n3:20109233
Subject Item
_:vb27795039
rdf:type
n2:Context
rdf:value
Injection of TLR-2 and TLR-4 enhanced myelin debris clearance and repairment of locomotor function after sciatic nerve lesion [>>93<<]. Blockade of TLRs and downstream signaling MyD88 decreased axons debris removal and delayed neuron regeneration [93]. MCP-1, macrophage inflammatory protein-1α, and interleukin-1β were reported to be involved in the progress of WD.
n2:mentions
n3:18003835
Subject Item
_:vb27795040
rdf:type
n2:Context
rdf:value
Blockade of TLRs and downstream signaling MyD88 decreased axons debris removal and delayed neuron regeneration [>>93<<]. MCP-1, macrophage inflammatory protein-1α, and interleukin-1β were reported to be involved in the progress of WD. Injection of these proinflammatory cytokines into the sciatic nerve led to rapid myelin damage and elevated
n2:mentions
n3:18003835
Subject Item
_:vb27795041
rdf:type
n2:Context
rdf:value
Injection of these proinflammatory cytokines into the sciatic nerve led to rapid myelin damage and elevated macrophage/microglial phagocytic activity in WD [>>94<<]. Efficient removal of degenerated neurons or cell debris is necessary to rebuild beneficial environment for neuronal regeneration in degenerated disease. In response to neuronal cell death, microglia become activated and aggregate around
n2:mentions
n3:15689362
Subject Item
_:vb27795042
rdf:type
n2:Context
rdf:value
In response to neuronal cell death, microglia become activated and aggregate around the lesioned area, exhibiting potent phagocytic activity [>>95<<]. Enhancement of myelin phagocytosis by microglial/macrophages favors neuron regeneration and restoration of locomotor function.
n2:mentions
n3:16337133
Subject Item
_:vb27795043
rdf:type
n2:Context
rdf:value
Immune effector cells including reactive microglia and hematogenous macrophages, as well as T cells, are observed aggregated in the lesion area in rat model of EAE [>>96<<, 97]. The exact mechanisms of demyelination remained unclear. Glial cell proliferation during the process of MS may be the major effector in the development of a demyelinating plaque due to the composition of the inflammation
n2:mentions
n3:11777538
Subject Item
_:vb27795044
rdf:type
n2:Context
rdf:value
Immune effector cells including reactive microglia and hematogenous macrophages, as well as T cells, are observed aggregated in the lesion area in rat model of EAE [96, >>97<<]. The exact mechanisms of demyelination remained unclear. Glial cell proliferation during the process of MS may be the major effector in the development of a demyelinating plaque due to the composition of the inflammation infiltrating, as
n2:mentions
n3:8530183
Subject Item
_:vb27795045
rdf:type
n2:Context
rdf:value
Glial cell proliferation during the process of MS may be the major effector in the development of a demyelinating plaque due to the composition of the inflammation infiltrating, as well as the dynamics of remyelination [>>98<<]. Early remyelinating lesions contained a mixture of infiltrated macrophages and microglia. Thin myelin sheaths were observed to surround the damaged axons [20, 34, 98], while in late remyelinating lesions only a few monomorphic
n2:mentions
n3:9775398
Subject Item
_:vb27795046
rdf:type
n2:Context
rdf:value
Thin myelin sheaths were observed to surround the damaged axons [>>20<<, 34, 98], while in late remyelinating lesions only a few monomorphic populations of phagocytic macrophages presented in these lesions [98].
n2:mentions
n3:9972873
Subject Item
_:vb27795047
rdf:type
n2:Context
rdf:value
Thin myelin sheaths were observed to surround the damaged axons [20, >>34<<, 98], while in late remyelinating lesions only a few monomorphic populations of phagocytic macrophages presented in these lesions [98].
n2:mentions
n3:17407101
Subject Item
_:vb27795048
rdf:type
n2:Context
rdf:value
Thin myelin sheaths were observed to surround the damaged axons [20, 34, >>98<<], while in late remyelinating lesions only a few monomorphic populations of phagocytic macrophages presented in these lesions [98].
n2:mentions
n3:9775398
Subject Item
_:vb27795049
rdf:type
n2:Context
rdf:value
Thin myelin sheaths were observed to surround the damaged axons [20, 34, 98], while in late remyelinating lesions only a few monomorphic populations of phagocytic macrophages presented in these lesions [>>98<<]. These studies suggested that insufficient myelin clearance in the CNS after MS onset may be involved in the failure of axonal regeneration. The relative contribution to disease progression of brain resident macrophages versus that of
n2:mentions
n3:9775398
Subject Item
_:vb27795050
rdf:type
n2:Context
rdf:value
viewpoint that resident macrophages play a decisive role in disease progression and selective depletion of perivascular and meningeal macrophages using clodronate liposome injection in rat model of acute EAE slows disease progression [>>96<<]. Recent studies using bone marrow chimeras claimed that the number of microglia were several folds over blood-derived macrophages, though they shared equal phagocytic capacity [97].
n2:mentions
n3:11777538
Subject Item
_:vb27795051
rdf:type
n2:Context
rdf:value
Recent studies using bone marrow chimeras claimed that the number of microglia were several folds over blood-derived macrophages, though they shared equal phagocytic capacity [>>97<<]. These findings support the hypothesis that microglia are more efficient in phagocytosing myelin debris compared with peripheral macrophages. In an in vitro Wallerian degeneration model by cutting axons of the cortical explants,
n2:mentions
n3:8530183
Subject Item
_:vb27795052
rdf:type
n2:Context
rdf:value
In an in vitro Wallerian degeneration model by cutting axons of the cortical explants, co-cultured microglia exposed to degenerated axon debris were first seen to engulf debris within15 h [>>99<<], whereas perivascular and meningeal macrophages infiltrating into the lesion area occurred at day 9 reached their maximum number at day 15 and decreased to normal level at day 24 post-EAE induction in rats [96].
n2:mentions
n3:19531468
Subject Item
_:vb27795053
rdf:type
n2:Context
rdf:value
engulf debris within15 h [99], whereas perivascular and meningeal macrophages infiltrating into the lesion area occurred at day 9 reached their maximum number at day 15 and decreased to normal level at day 24 post-EAE induction in rats [>>96<<]. The different types of macrophage activation in MS/EAE are closely correlated with the stage of the demyelinating activity and with the type of MS tissue [99].
n2:mentions
n3:11777538
Subject Item
_:vb27795054
rdf:type
n2:Context
rdf:value
The different types of macrophage activation in MS/EAE are closely correlated with the stage of the demyelinating activity and with the type of MS tissue [>>99<<]. In early-active MS lesion, massive activated macrophages aggregated at the plaque border and engaged in phagocytosing myelin degradation products; however, in late-active demyelination lesion, a small number of amoeboid-like macrophages
n2:mentions
n3:19531468
Subject Item
_:vb27795055
rdf:type
n2:Context
rdf:value
aggregated at the plaque border and engaged in phagocytosing myelin degradation products; however, in late-active demyelination lesion, a small number of amoeboid-like macrophages were observed diffusely infiltrated in the lesion [>>98<<, 99]. The brain resident microglia are the main macrophages engaged in phagocytosis in the early stage of demyelination, while in the late stage a number of infiltrated blood-borne macrophages contribute to axon debris clearance.
n2:mentions
n3:9775398
Subject Item
_:vb27795056
rdf:type
n2:Context
rdf:value
aggregated at the plaque border and engaged in phagocytosing myelin degradation products; however, in late-active demyelination lesion, a small number of amoeboid-like macrophages were observed diffusely infiltrated in the lesion [98, >>99<<]. The brain resident microglia are the main macrophages engaged in phagocytosis in the early stage of demyelination, while in the late stage a number of infiltrated blood-borne macrophages contribute to axon debris clearance.
n2:mentions
n3:19531468
Subject Item
_:vb27795057
rdf:type
n2:Context
rdf:value
A variety of types of receptors are involved in MS, including Fc receptors, complement receptors, macrophage scavenger receptors, the galectin-3/MAC-2 receptors, α2-macroglobulin/low-density lipoprotein receptor, and mannose receptors [>>8<<]. In these receptor-linked pathways, TREM-2 signaling pathway has been the most well-studied.
n2:mentions
n3:19409897
Subject Item
_:vb27795058
rdf:type
n2:Context
rdf:value
TREM-2 mediated phagocytosis of apoptotic neurons without release of pro-inflammation molecules in animal model of MS [>>35<<, 100]. Han et al. recently demonstrated that downregulation of CD47 promoted phagocytosis of myelin in a SIRP-α-dependent mechanism by using CD47−/− EAE mice [101]. The capacity of macrophages/microglia to phagocytose degenerated myelin
n2:mentions
n3:15728241
Subject Item
_:vb27795059
rdf:type
n2:Context
rdf:value
TREM-2 mediated phagocytosis of apoptotic neurons without release of pro-inflammation molecules in animal model of MS [35, >>100<<]. Han et al. recently demonstrated that downregulation of CD47 promoted phagocytosis of myelin in a SIRP-α-dependent mechanism by using CD47−/− EAE mice [101]. The capacity of macrophages/microglia to phagocytose degenerated myelin can be
n2:mentions
n3:8933159
Subject Item
_:vb27795060
rdf:type
n2:Context
rdf:value
Han et al. recently demonstrated that downregulation of CD47 promoted phagocytosis of myelin in a SIRP-α-dependent mechanism by using CD47−/− EAE mice [>>101<<]. The capacity of macrophages/microglia to phagocytose degenerated myelin can be altered by environmental inflammatory mediators, such as IFN-γ, TNF-α, IL-4, IL-10, and so on [20]. This notion was confirmed by an in vitro study that
n2:mentions
n3:22734047
Subject Item
_:vb27795061
rdf:type
n2:Context
rdf:value
The capacity of macrophages/microglia to phagocytose degenerated myelin can be altered by environmental inflammatory mediators, such as IFN-γ, TNF-α, IL-4, IL-10, and so on [>>20<<]. This notion was confirmed by an in vitro study that investigated the effect of certain cytokines on phagocytosis of 14C-labeled myelin by cultured macrophages or microglia. In this study, TNF-α was shown to increase the phagocytic
n2:mentions
n3:9972873
Subject Item
_:vb27795062
rdf:type
n2:Context
rdf:value
In this study, TNF-α was shown to increase the phagocytic activity of microglia, but have no effect on macrophages [>>20<<]. TNF-γ was demonstrated to reduce removal of myelin by macrophage, on the contrary enhance debris clearance driven by microglia. IL-4 and IL-10 exerted a role of up-regulating phagocytosis in macrophages/microglia, while accompanied by a
n2:mentions
n3:9972873
Subject Item
_:vb27795063
rdf:type
n2:Context
rdf:value
IL-4 and IL-10 exerted a role of up-regulating phagocytosis in macrophages/microglia, while accompanied by a reduction of inflammatory response [>>20<<]. In demyelinated diseases, efficient removal of degenerated myelin is necessary to rebuild beneficial environment for remyelination and axon regeneration. Therefore, robust microglial phagocytosis might be critical in the recovery of
n2:mentions
n3:9972873
Subject Item
_:vb27795064
rdf:type
n2:Context
rdf:value
Macrophages/microglia were observed to present in tumors, tumor periphery, and contralateral tumor-free hemispheres, particularly around tumor margins [>>102<<, 103]. Badie and Schartner revealed that infiltrated microglia comprise 13.2 to 34.0 % of tumor mass, and the extent of microglia infiltration depends on the tumor type rather than its size [102]. Glioma-infiltrating microglia/macrophages
n2:mentions
n3:10764271
Subject Item
_:vb27795065
rdf:type
n2:Context
rdf:value
Macrophages/microglia were observed to present in tumors, tumor periphery, and contralateral tumor-free hemispheres, particularly around tumor margins [102, >>103<<]. Badie and Schartner revealed that infiltrated microglia comprise 13.2 to 34.0 % of tumor mass, and the extent of microglia infiltration depends on the tumor type rather than its size [102]. Glioma-infiltrating microglia/macrophages show
n2:mentions
n3:23331472
Subject Item
_:vb27795066
rdf:type
n2:Context
rdf:value
Badie and Schartner revealed that infiltrated microglia comprise 13.2 to 34.0 % of tumor mass, and the extent of microglia infiltration depends on the tumor type rather than its size [>>102<<]. Glioma-infiltrating microglia/macrophages show protumorigenic activity by upregulation of metalloprotease-II [104], but cannot secrete cytokines such as IL-1β, IL-6, and TNF-α, which is distinctive from the inflammatory phenotype [105].
n2:mentions
n3:10764271
Subject Item
_:vb27795067
rdf:type
n2:Context
rdf:value
Glioma-infiltrating microglia/macrophages show protumorigenic activity by upregulation of metalloprotease-II [>>104<<], but cannot secrete cytokines such as IL-1β, IL-6, and TNF-α, which is distinctive from the inflammatory phenotype [105].
n2:mentions
n3:16141784
Subject Item
_:vb27795068
rdf:type
n2:Context
rdf:value
Glioma-infiltrating microglia/macrophages show protumorigenic activity by upregulation of metalloprotease-II [104], but cannot secrete cytokines such as IL-1β, IL-6, and TNF-α, which is distinctive from the inflammatory phenotype [>>105<<]. In glioma microenvironment, normal human astrocytes (NHA), glioma cells, and microglia all show capability of phagocytosing glioma cells and specifically apoptotic tumor cells [106].
n2:mentions
n3:17965659
Subject Item
_:vb27795069
rdf:type
n2:Context
rdf:value
In glioma microenvironment, normal human astrocytes (NHA), glioma cells, and microglia all show capability of phagocytosing glioma cells and specifically apoptotic tumor cells [>>106<<]. The phagocytosis index (the index to assess the phagocytic activity of phagocytes through counting of engulfed apoptotic cells) value of microglia showed about four-fold higher than that of NHA or glioma cells, indicating that microglia
n2:mentions
n3:11302338
Subject Item
_:vb27795070
rdf:type
n2:Context
rdf:value
activity of phagocytes through counting of engulfed apoptotic cells) value of microglia showed about four-fold higher than that of NHA or glioma cells, indicating that microglia were the most efficient phagocytes in brain tumor [>>106<<]. IL-12 and LPS administration obviously enhance microglial phagocytotic activity through the TRAIL pathway [107].
n2:mentions
n3:11302338
Subject Item
_:vb27795071
rdf:type
n2:Context
rdf:value
IL-12 and LPS administration obviously enhance microglial phagocytotic activity through the TRAIL pathway [>>107<<]. In vitro study revealed that glioma cancer stem cells (gCSCs) dramatically inhibited phagocytosis by human microglia [108]. Further study regarding underlying mechanisms showed reversal of phagocytosis inhibition after STAT3 blockade by
n2:mentions
n3:21399879
Subject Item
_:vb27795072
rdf:type
n2:Context
rdf:value
In vitro study revealed that glioma cancer stem cells (gCSCs) dramatically inhibited phagocytosis by human microglia [>>108<<]. Further study regarding underlying mechanisms showed reversal of phagocytosis inhibition after STAT3 blockade by WP1066 and STAT3 siRNA in gCSCs, suggesting involvement of p-STAT3 pathway in inhibition of phagocytosis by gCSCs [108].
n2:mentions
n3:20667896
Subject Item
_:vb27795073
rdf:type
n2:Context
rdf:value
Further study regarding underlying mechanisms showed reversal of phagocytosis inhibition after STAT3 blockade by WP1066 and STAT3 siRNA in gCSCs, suggesting involvement of p-STAT3 pathway in inhibition of phagocytosis by gCSCs [>>108<<]. Microglia play a key role in phagocytosing tumor cells. This activity can be modulated by cancer cells or cancer environment. Whether microglial phagocytosis serves as cancer defense or cancer contribution still needs further
n2:mentions
n3:20667896
Subject Item
_:vb27795074
rdf:type
n2:Context
rdf:value
Studies have shown that immune response is pivotal in prion disease [>>9<<, 109–112]. In prion disease, microglia become activated and take a decisive role in the progression of this disease [9].
n2:mentions
n3:11455614
Subject Item
_:vb27795075
rdf:type
n2:Context
rdf:value
Studies have shown that immune response is pivotal in prion disease [9, >>109<<–112]. In prion disease, microglia become activated and take a decisive role in the progression of this disease [9].
n2:mentions
n3:20878768 n3:20609379 n3:19779137 n3:20837697
Subject Item
_:vb27795076
rdf:type
n2:Context
rdf:value
In prion disease, microglia become activated and take a decisive role in the progression of this disease [>>9<<]. Microglia in prion disease displayed low level of secretory profiles and elevated expression of phagocytotic machinery such as receptors for advanced glycation end products, TREM-2, and the scavenger receptors SAR2, CD68, and SRB(CD36)
n2:mentions
n3:11455614
Subject Item
_:vb27795077
rdf:type
n2:Context
rdf:value
in prion disease displayed low level of secretory profiles and elevated expression of phagocytotic machinery such as receptors for advanced glycation end products, TREM-2, and the scavenger receptors SAR2, CD68, and SRB(CD36) [>>109<<]. It is striking that intracerebral injection of LPS significantly stimulated synthesis and secretion of proinflammatory cytokines, but without alteration of PrPs clearance [109], which is thoroughly different from the generally accepted
n2:mentions
n3:20878768
Subject Item
_:vb27795078
rdf:type
n2:Context
rdf:value
It is striking that intracerebral injection of LPS significantly stimulated synthesis and secretion of proinflammatory cytokines, but without alteration of PrPs clearance [>>109<<], which is thoroughly different from the generally accepted notion that microglial phagocytic state is positively in line with its activation degree [113].
n2:mentions
n3:20878768
Subject Item
_:vb27795079
rdf:type
n2:Context
rdf:value
secretion of proinflammatory cytokines, but without alteration of PrPs clearance [109], which is thoroughly different from the generally accepted notion that microglial phagocytic state is positively in line with its activation degree [>>113<<]. Numerous findings demonstrated that microglia also participated in radiation induced neuronal damage [114–119].
n2:mentions
n3:10407127
Subject Item
_:vb27795080
rdf:type
n2:Context
rdf:value
Numerous findings demonstrated that microglia also participated in radiation induced neuronal damage [>>114<<–119]. Microglia with phagocytic morphology could be seen accumulated in the lesion cavity/spinal cord interface in irradiated spinal cord hemisection. Interestingly, microglial population rapidly decreased in the irradiated, lesioned
n2:mentions
n3:19056908 n3:12821387 n3:20617366 n3:19670439 n3:19070908
Subject Item
_:vb27795081
rdf:type
n2:Context
rdf:value
Interestingly, microglial population rapidly decreased in the irradiated, lesioned hemisection when compared to nonirradiated animal [>>114<<, 118]. However, the exact mechanism underlying phagocytic process and the role of clearance by microglia in radiation induced brain injury needs further investigation.
n2:mentions
n3:19070908
Subject Item
_:vb27795082
rdf:type
n2:Context
rdf:value
Interestingly, microglial population rapidly decreased in the irradiated, lesioned hemisection when compared to nonirradiated animal [114, >>118<<]. However, the exact mechanism underlying phagocytic process and the role of clearance by microglia in radiation induced brain injury needs further investigation.
n2:mentions
n3:12821387
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