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Expression of complement C4 and C9 genes by human astrocytes.

Authors
Walker, DG; Kim, SU; McGeer, PL
Citation
Brain research, 809(1):31-38, 1998
Journal Title
Brain research
ISSN
0006-89931872-6240
Abstract
Evidence exists that complement activation is involved in the pathogenesis of Alzheimer's disease (AD). It has been previously demonstrated that central nervous system (CNS) resident cells can synthesize complement proteins. Two key proteins in the complement pathway are the complement C4 and C9 proteins. Using reverse transcription-polymerase chain reaction, ELISA, immunocytochemical and immunoblot techniques, we showed that primary human astrocytes constitutively expressed complement C4 mRNA and protein, and that this was increased when cells were treated with interferon-gamma, but inhibited when cells were treated with interleukin-1beta (IL-1beta). C4 immunoreactivity could be localized to GFAP-positive astrocytes when protein secretion was inhibited. These results indicated that astrocytes could be a source of complement C4 in the human CNS. In addition it was shown that stimulated astrocytes could also express complement C9 mRNA, though C9 protein was not detectable in culture supernatants.
MeSH terms
Astrocytes/chemistry/cytology/*physiologyCells, CulturedComplement C4/analysis/*genetics/secretionComplement C9/analysis/*geneticsEnzyme-Linked Immunosorbent AssayFetus/cytologyGene Expression/drug effects/physiologyHumansInterferon-gamma/pharmacologyInterleukin-1/pharmacologyRNA, Messenger/analysis
PMID
9795119
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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