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1 Division of Nephrology, Departments of Medicine and Pathology, University of Washington, Seattle, Washington, 98195; and 2 University of Tokyo, Tokyo 113-8655, Japan
We studied
the role of the C5b-9 membrane attack complex in two models of
inflammatory glomerulonephritis (GN) initiated by acute glomerular
endothelial injury in Piebold-viral-Glaxo (PVG) complement-sufficient
rats (C+), C6-deficient rats (C6
), and rats systematically
depleted of complement with cobra venom factor (CVF). GN was induced by
performing a left nephrectomy and selectively perfusing the right
kidney with either 1) the lectin concanavalin A (Con A)
followed by complement-fixing anti-Con A (Con A GN) or 2)
purified complement-fixing goat anti-rat glomerular endothelial cell
(GEN) antibody [immune-mediated thrombotic microangiopathy (ITM)]. Comparable levels of GEN apoptosis were detected in C+ animals in both models. CVF administration reduced GEN apoptosis by 10- to 12-fold. GEN apoptosis was C5b-9 dependent because PVG C6
rats were protected from GEN loss. Furthermore, functional inhibition
of the cell surface complement regulatory protein CD59 by renal
perfusion with anti-CD59 antibody in ITM resulted in a 3.5-fold
increase in GEN apoptosis. Last, in Con A GN, abrogation of GEN
apoptosis preserved endothelial integrity and renal function. This
study demonstrates the specific role of C5b-9 in the induction of GEN
apoptosis in experimental inflammatory GN, a finding with implications
for diseases associated with the presence of antiendothelial cell antibodies.
complement; inflammation; cell death
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