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Originally published In Press as doi:10.1074/jbc.M109546200 on January 23, 2002

J. Biol. Chem., Vol. 277, Issue 15, 13029-13036, April 12, 2002
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Cyclooxygenase-2 Is Induced in Monocytes by Peroxisome Proliferator Activated Receptor gamma  and Oxidized Alkyl Phospholipids from Oxidized Low Density Lipoprotein*

Aaron V. PontslerDagger §, Andy St. HilaireDagger §, Gopal K. MaratheDagger §, Guy A. ZimmermanDagger §, and Thomas M. McIntyreDagger §||

From the Departments of  Pathology, § Internal Medicine, Dagger  Human Molecular Biology and Genetics Program, University of Utah, Salt Lake City, Utah 84112

Low density lipoprotein (LDL) oxidation and monocyte infiltration of the vessel wall underlie atherogenesis. These cells express cyclooxygenase-2, but the way oxidized LDL stimulates cyclooxygenase-2 transcription is unknown. Oxidized LDL, oxidatively fragmented phospholipids isolated from oxidized LDL, a synthetic oxidized alkylphospholipid (azPC) that is a potent peroxisome proliferator activated receptor (PPAR) gamma  agonist, or the PPARgamma agonist rosiglitazone all induced cyclooxygenase-2 expression and enhanced prostaglandin E2 (PGE2) secretion in primary human monocytes. The cyclooxygenase-2 inhibitor NS398 blocked PPARgamma -induced PGE2 secretion. Phospholipase A1 and A2 digestion shows that oxidized alkylphospholipids, and not oxidized fatty acids, were the relevant agonists. The upstream PPAR-responsive element (PPRE) of cyclooxygenase-2 was required for induction of a luciferase reporter by oxidized phospholipids, azPC, and rosiglitazone, and a (COX-2 PPRE)3-luciferase reporter was responsive to these PPARgamma agonists. Circulating human monocytes do not contain PPARgamma , but PPARgamma was induced rapidly (<4 h) in monocytes upon ligation of surface ICAM-3, but not P-selectin glycoprotein-1 even though both interactions prime cytokine secretion. Cyclooxygenase-2 induction by oxidized phospholipids only occurred in monocytes containing PPARgamma . Thus PPARgamma was induced rapidly in primary monocytes by appropriate outside-in signaling, sensitizing them to previously undetectable agonists in oxidized LDL. Cyclooxygenase-2 and PGE2 secretion are induced, not inhibited, by selective PPARgamma agonists that include oxidatively fragmented phospholipids in oxidized LDL.

* This work was supported by National Institutes of Health Grants HL44513, HL50153, and HL44525.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: 4130 EIHG, 15 North 2030 East, University of Utah, Salt Lake City, UT 84112-5330. Tel.: 801-585-0716; Fax: 801-585-0701; E-mail: tom.mcintyre@hmbg.utah.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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