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• W53296430 startingPage "2091" @default.
• W53296430 abstract "In the passive Heymann nephritis (PHN) model of membranous nephropathy, complement C5b-9 induces glomerular epithelial cell (GEC) injury and proteinuria, which is partially mediated by eicosanoids. This study addresses the role of cyclooxygenase (COX)-1 and -2 in C5b-9-mediated eicosanoid production in GEC. Unstimulated rat GEC in culture primarily express COX-1. When stimulated with sublytic C5b-9, COX-2 was significantly up-regulated, whereas COX-1 was not affected. Compared with control, complement-treated GEC produced 32% more prostaglandin (PG) E(2) in the presence of exogenous substrate, and the increase was abolished with the COX-2-selective inhibitor, NS-398. Release of arachidonic acid from GEC phospholipids via C5b-9-induced activation of cytosolic phospholipase A(2) was associated with a marked stimulation of PGE(2) production, which was inhibited by 60% with NS-398. The results in cultured GEC were extended to GEC injury in vivo by examining COX-1 and -2 expression in PHN. Glomeruli from rats with PHN expressed significantly more COX-1 and COX-2, as compared with normal rats. PGE(2) production in glomeruli of rats with PHN was about twofold greater than in control glomeruli, and the increase was partially inhibited with NS-398. Thus, in GEC in culture and in vivo, C5b-9-induced eicosanoid production is regulated by both isoforms of COX. The inducible COX-2 may be an important novel mediator of C5b-9-induced glomerular injury." @default.
• W53296430 created "2016-06-24" @default.
• W53296430 creator A5043984170 @default.
• W53296430 creator A5057779986 @default.
• W53296430 date "2000-06-01" @default.
• W53296430 modified "2023-10-15" @default.
• W53296430 title "Complement C5b-9-Mediated Arachidonic Acid Metabolism in Glomerular Epithelial Cells" @default.
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• W53296430 doi "https://doi.org/10.1016/s0002-9440(10)65080-8" @default.
• W53296430 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1850096" @default.
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