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CD36 Regulates Oxidative Stress and Inflammation in Hypercholesterolemic CKD

Daryl M. Okamura^*, Subramaniam Pennathur, Katie Pasichnyk^*, Jesús M. López-Guisa^*, Sarah Collins^*, Maria Febbraio, Jay Heinecke and Allison A. Eddy^*

^* Department of Pediatrics, Seattle Children's Research Institute, and Department of Endocrinology and Metabolism, University of Washington, Seattle, Washington; Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan; and Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio

Correspondence: Dr. Daryl M. Okamura, Seattle Children's Research Institute, Division of Nephrology, 4800 Sand Point Way NE, A7931, Seattle, WA 98105. Phone: 206-987-2524; Fax: 206-987-2636; E-mail: daryl.okamura{at}seattlechildrens.org

Received for publication January 4, 2008. Accepted for publication October 15, 2008.

Scavenger receptors play a central role in atherosclerosis by processing oxidized lipoproteins and mediating their cellular effects. Recent studies suggested that the atherogenic state correlates with progression of chronic kidney disease (CKD); therefore, scavenger receptors are candidate mediators of renal fibrogenesis. Here, we investigated the role of CD36, a class B scavenger receptor, in a hypercholesterolemic model of CKD. We placed CD36-deficient mice and wild-type male mice on a high-fat Western diet for 7 to 8 wk and then performed either sham or unilateral ureteral obstruction surgery. CD36-deficient mice developed significantly less fibrosis compared with wild-type mice at days 3, 7, and 14 after obstruction. Compared with wild-type mice, CD36-deficient mice had significantly more interstitial macrophages at 7 d but not at 14 d. CD36-deficient mice exhibited reduced levels of activated NF-B and oxidative stress (assessed by measuring fatty acid–derived hydroxyoctadecadienoic acid and protein carbonyl content) and decreased accumulation of interstitial myofibroblasts compared with wild-type mice. These data suggest that CD36 is a key modulator of proinflammatory and oxidative pathways that promote fibrogenesis in CKD.

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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673