NDLI: Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusion

Content Provider	PubMed Central
Author	Thurman, Joshua M. Ljubanović, Danica Royer, Pamela A. Kraus, Damian M. Molina, Hector Barry, Nicholas P. Proctor, Gregory Levi, Moshe Michael, Holers V.
Copyright Year	2006
Abstract	Ischemia/reperfusion (I/R) of several organs results in complement activation, but the kidney is unique in that activation after I/R occurs only via the alternative pathway. We hypothesized that selective activation of this pathway after renal I/R could occur either because of a loss of complement inhibition or from increased local synthesis of complement factors. We examined the relationship between renal complement activation after I/R and the levels and localization of intrinsic membrane complement inhibitors. We found that loss of polarity of complement receptor 1–related protein y (Crry) in the tubular epithelium preceded activation of the alternative pathway along the basolateral aspect of the tubular cells. Heterozygous gene-targeted mice that expressed lower amounts of Crry were more sensitive to ischemic injury. Furthermore, inhibition of Crry expressed by proximal tubular epithelial cells in vitro resulted in alternative pathway–mediated injury to the cells. Thus, altered expression of a complement inhibitor within the tubular epithelium appears to be a critical factor permitting activation of the alternative pathway of complement after I/R. Increased C3 mRNA and decreased factor H mRNA were also detected in the outer medulla after I/R, suggesting that altered synthesis of these factors might further contribute to complement activation in this location.
Related Links	http://dx.doi.org/10.1172/jci24521
Ending Page	368
Page Count	12
Starting Page	357
File Format	PDF
ISSN	00219738
Journal	Journal of Clinical Investigation
Issue Number	2
Volume Number	116
Language	English
Publisher	American Society for Clinical Investigation
Publisher Date	2006-01-01
Access Restriction	Open
Rights Holder	American Society for Clinical Investigation
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine

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