Differential expression of interferon-gamma receptor on human glial cells in vivo and in vitro.
Identifieur interne : 001A65 ( Main/Exploration ); précédent : 001A64; suivant : 001A66Differential expression of interferon-gamma receptor on human glial cells in vivo and in vitro.
Auteurs : Sadayuki Hashioka [Canada] ; Andis Klegeris ; Claudia Schwab ; Sheng Yu ; Patrick L. McgeerSource :
- Journal of neuroimmunology [ 1872-8421 ] ; 2010.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (pathology), Amyotrophic Lateral Sclerosis (pathology), Brain (cytology), Brain (pathology), Cells, Cultured, DNA-Binding Proteins (metabolism), Female, Gene Expression Regulation (genetics), Gene Expression Regulation (physiology), Glial Fibrillary Acidic Protein (metabolism), Humans, Male, Middle Aged, Myelin Basic Protein (metabolism), Neuroglia (metabolism), Parkinson Disease (pathology), Receptors, Interferon (genetics), Receptors, Interferon (metabolism), Spinal Cord (cytology), Spinal Cord (pathology).
- MESH :
- chemical , genetics : Receptors, Interferon.
- chemical , metabolism : DNA-Binding Proteins, Glial Fibrillary Acidic Protein, Myelin Basic Protein, Receptors, Interferon.
- cytology : Brain, Spinal Cord.
- genetics : Gene Expression Regulation.
- metabolism : Neuroglia.
- pathology : Alzheimer Disease, Amyotrophic Lateral Sclerosis, Brain, Parkinson Disease, Spinal Cord.
- physiology : Gene Expression Regulation.
- Aged, Aged, 80 and over, Cells, Cultured, Female, Humans, Male, Middle Aged.
Abstract
Although significant effects of interferon-gamma (IFN-gamma) on glial cells are well documented, information on the expression level and localization of glial IFN-gamma receptors (IFN-gamma-R) in the human central nervous system (CNS) is sparse. To examine the glial expression of IFN-gamma-R in the human CNS, immunohistochemistry and quantitative analyses were performed on Alzheimer disease hippocampus, Parkinson disease substantia nigra, amyotrophic lateral sclerosis spinal cord and corresponding areas from non-neurological cases. Almost all IFN-gamma-R-positive (IFN-gamma-R(+)) cells corresponded to GFAP-positive (GFAP(+)) astrocytes, while none of IFN-gamma-R(+) cells corresponded to IBA1-positive (IBA1(+)) microglia or MBP-positive (MBP(+)) oligodendrocytes in these neurological cases. We observed a similar pattern of glial IFN-gamma-R expression in non-neurological cases. Also, we quantitatively analyzed the IFN-gamma-R expression by cultured human glial cells using immunocytochemistry and reverse transcription polymerase chain reaction (RT-PCR). In contrast to in vivo results, almost all IFN-gamma-R(+) cells were IBA1(+) in microglial cultures, GFAP(+) in astrocytic cultures and MBP(+) in oligodendrocytic cultures. Moreover, no significant difference in IFN-gamma-R mRNA expression was found for these glial cell types by RT-PCR. These results suggest that the microglial and oligodendrocytic expression levels of IFN-gamma-R are much lower than the astrocytic expression levels in the human CNS in vivo, whereas all three types of glial cells constitutively express IFN-gamma-R when cultured in vitro.
DOI: 10.1016/j.jneuroim.2010.04.023
PubMed: 20554027
Affiliations:
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Mcgeer</name></author></analytic><series><title level="j">Journal of neuroimmunology</title><idno type="eISSN">1872-8421</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (pathology)</term><term>Amyotrophic Lateral Sclerosis (pathology)</term><term>Brain (cytology)</term><term>Brain (pathology)</term><term>Cells, Cultured</term><term>DNA-Binding Proteins (metabolism)</term><term>Female</term><term>Gene Expression Regulation (genetics)</term><term>Gene Expression Regulation (physiology)</term><term>Glial Fibrillary Acidic Protein (metabolism)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Myelin Basic Protein (metabolism)</term><term>Neuroglia (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Receptors, Interferon (genetics)</term><term>Receptors, Interferon (metabolism)</term><term>Spinal Cord (cytology)</term><term>Spinal Cord (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Interferon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DNA-Binding Proteins</term><term>Glial Fibrillary Acidic Protein</term><term>Myelin Basic Protein</term><term>Receptors, Interferon</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Brain</term><term>Spinal Cord</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neuroglia</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Amyotrophic Lateral Sclerosis</term><term>Brain</term><term>Parkinson Disease</term><term>Spinal Cord</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although significant effects of interferon-gamma (IFN-gamma) on glial cells are well documented, information on the expression level and localization of glial IFN-gamma receptors (IFN-gamma-R) in the human central nervous system (CNS) is sparse. To examine the glial expression of IFN-gamma-R in the human CNS, immunohistochemistry and quantitative analyses were performed on Alzheimer disease hippocampus, Parkinson disease substantia nigra, amyotrophic lateral sclerosis spinal cord and corresponding areas from non-neurological cases. Almost all IFN-gamma-R-positive (IFN-gamma-R(+)) cells corresponded to GFAP-positive (GFAP(+)) astrocytes, while none of IFN-gamma-R(+) cells corresponded to IBA1-positive (IBA1(+)) microglia or MBP-positive (MBP(+)) oligodendrocytes in these neurological cases. We observed a similar pattern of glial IFN-gamma-R expression in non-neurological cases. Also, we quantitatively analyzed the IFN-gamma-R expression by cultured human glial cells using immunocytochemistry and reverse transcription polymerase chain reaction (RT-PCR). In contrast to in vivo results, almost all IFN-gamma-R(+) cells were IBA1(+) in microglial cultures, GFAP(+) in astrocytic cultures and MBP(+) in oligodendrocytic cultures. Moreover, no significant difference in IFN-gamma-R mRNA expression was found for these glial cell types by RT-PCR. These results suggest that the microglial and oligodendrocytic expression levels of IFN-gamma-R are much lower than the astrocytic expression levels in the human CNS in vivo, whereas all three types of glial cells constitutively express IFN-gamma-R when cultured in vitro.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Klegeris, Andis" sort="Klegeris, Andis" uniqKey="Klegeris A" first="Andis" last="Klegeris">Andis Klegeris</name><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name><name sortKey="Schwab, Claudia" sort="Schwab, Claudia" uniqKey="Schwab C" first="Claudia" last="Schwab">Claudia Schwab</name><name sortKey="Yu, Sheng" sort="Yu, Sheng" uniqKey="Yu S" first="Sheng" last="Yu">Sheng Yu</name></noCountry><country name="Canada"><noRegion><name sortKey="Hashioka, Sadayuki" sort="Hashioka, Sadayuki" uniqKey="Hashioka S" first="Sadayuki" last="Hashioka">Sadayuki Hashioka</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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