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Originally published In Press as doi:10.1074/jbc.M011663200 on March 5, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17030-17035, May 18, 2001
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Mitogen-activated Protein Kinase Phosphatase 1 Activity Is Necessary for Oxidized Phospholipids to Induce Monocyte Chemotactic Activity in Human Aortic Endothelial Cells*

Srinivasa ReddyDagger §, Susan HamaDagger , Victor GrijalvaDagger , Khaled HassanDagger , Rachel MottahedehDagger , Greg HoughDagger , David J. WadleighDagger , Mohamad NavabDagger , and Alan M. FogelmanDagger

From the Atherosclerosis Research Unit, Dagger  Department of Medicine, and § Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California 90095-1679

Entrapment and oxidation of low density lipoproteins (LDL) in the sub-endothelial space is a key process in the initiation of atherosclerotic lesion development. Functional changes induced by oxidized lipids in endothelial cells are early events in the pathogenesis of atherosclerosis. Oxidized-L-alpha -1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (ox-PAPC), a major component of minimally modified/oxidized-LDL (MM-LDL) mimics the biological activities assigned to MM-LDL both in vitro in a co-culture model as well as in vivo in mice. We hypothesized that ox-PAPC initiates gene expression changes in endothelial cells that result in enhanced endothelial/monocyte interactions. To analyze the gene expression changes that oxidized lipids induce in endothelial cells, we used a suppression subtractive hybridization procedure to compare mRNA from PAPC-treated human aortic endothelial cells (HAEC) with that of ox-PAPC-treated cells. We report here the identification of a gene, mitogen-activated protein kinase phosphatase 1 (MKP-1), that is rapidly and transiently induced in ox-PAPC-treated HAEC. Inhibition of MKP-1 using either the phosphatase inhibitor sodium orthovanadate or antisense oligonucleotides prevents the accumulation of monocyte chemotactic activity in ox-PAPC-treated HAEC supernatants. Furthermore, we show that decreased monocyte chemotactic activity in HAEC treated with sodium orthovanadate or MKP-1 antisense oligonucleotides is due to decreased MCP-1 protein. Our results implicate a direct role for MKP-1 in ox-PAPC-induced signaling pathways that result in the production of MCP-1 protein by ox-PAPC-treated HAEC.

* This work was supported by United States Public Health Service Grant HL 30568, a Tobacco Related Disease Research Project grant from the State of California, and the Laubisch, Castera, and M. K. Gray Fund at UCLA.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: Dept. of Medicine and Dept. of Molecular and Medical Pharmacology, University of California Los Angeles, 650 Charles E. Young Dr. South, A8-131, CHS, Los Angeles, CA 90095. Tel.: 310-206--3915; Fax: 310-206-3605; E-mail: sreddy@mednet.ucla.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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