Expression of the complement C3a and C5a receptors after permanent focal ischemia: An alternative interpretation
The receptors for the complement anaphylatoxins C3a and C5a are expressed by glial cells and neurons in normal and inflamed brain. Previous studies demonstrated modest elevations in mRNA expression of these receptors in a model of focal cerebral ischemia. Using a similar model system for both mice a...
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Published in | Glia Vol. 38; no. 2; pp. 169 - 173 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Wiley Subscription Services, Inc., A Wiley Company
15.04.2002
Wiley-Liss |
Subjects | |
Online Access | Get full text |
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Summary: | The receptors for the complement anaphylatoxins C3a and C5a are expressed by glial cells and neurons in normal and inflamed brain. Previous studies demonstrated modest elevations in mRNA expression of these receptors in a model of focal cerebral ischemia. Using a similar model system for both mice and rats, we report markedly different patterns of anaphylatoxin receptor mRNA expression in cerebral ischemia. C5a receptor expression was dramatically elevated within 3 h after middle cerebral artery occlusion, while C3aR expression was reduced to 25% of control animals. By 24 h post‐occlusion, expression of both receptors was higher than at any other time point examined. This increased expression at late time points after occlusion is most likely the result of massive infiltration of leukocytes expressing the receptors. We also observed increased receptor mRNA expression in sham‐operated animals, indicating that the procedures used for arterial occlusion affects mechanisms regulating receptor expression. This latter result highlights the importance of including this important control group in ischemic model systems for proper interpretation of changes in gene expression. GLIA 38:169–173, 2002. © 2002 Wiley‐Liss, Inc. |
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Bibliography: | ark:/67375/WNG-QP8KMDK4-B istex:58AC54499449E494425A24F0365B1A6D100EF2A1 ArticleID:GLIA10069 National Institutes of Health - No. NS29717 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0894-1491 1098-1136 |
DOI: | 10.1002/glia.10069 |