© 2000 American Heart Association, Inc.
Molecular Medicine |
Role for Peroxisome Proliferator-Activated Receptor 
in Oxidized Phospholipid–Induced Synthesis of Monocyte Chemotactic Protein-1 and Interleukin-8 by Endothelial Cells
From the Division of Cardiology (H.L., W.S., S.W., G.S., L.H., S.H., C.B., J.A.B.), Department of Medicine, and Department of Pathology (J.A.B.), University of California, Los Angeles; The Salk Institute of Biological Studies (P.T., R.M.E., L.N.); and Howard Hughes Medical Institute (R.M.E.), La Jolla, Calif. Present address for L.N. is University of Debrecen, Medical and Health Science Center, Department of Biochemistry and Molecular Biology, Debrecen, Hungary; present address for P.T. is Department of Pathology, University of California, Los Angeles.
Correspondence to Judith A. Berliner, PhD, Department of Pathology and Medicine, UCLA School of Medicine, 13-239 Center for the Health Sciences, 650 Charles Young Dr, Los Angeles, CA 90095-1732. E-mail jberliner{at}mednet.ucla.edu
Abstract—The attraction, binding,
and entry of monocytes into the vessel wall play an important role in
atherogenesis. We have previously shown that minimally
oxidized/modified LDL (MM-LDL), a pathogenically relevant lipoprotein,
can activate human aortic endothelial cells
(HAECs) to produce monocyte chemotactic activators. In the
present study, we demonstrate that MM-LDL and oxidation
products of
1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphocholine
(PAPC) activate endothelial cells to synthesize
monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8).
Several lines of evidence suggest that this activation is mediated by
the lipid-dependent transcription factor peroxisome
proliferator-activated receptor 
(PPAR), the most
abundant member of the PPAR family in HAECs. Treatment of transfected
CV-1 cells demonstrated activation of the PPAR ligand-binding domain
by MM-LDL, Ox-PAPC, or its component phospholipids,
1-palmitoyl-2-oxovalaroyl-sn-glycero-phosphocholine and
1-palmitoyl-2-glutaroyl-sn-glycero-phosphocholine; these
lipids also activated a consensus peroxisome
proliferator-activated receptor response element (PPRE) in transfected
HAECs. Furthermore, activation of PPAR with synthetic ligand
Wy14,643 stimulates the synthesis of IL-8 and MCP-1 by HAECs. By
contrast, troglitazone, a PPAR
agonist, decreased the levels of IL-8
and MCP-1. Finally, we demonstrate that unlike wild-type
endothelial cells, endothelial cells
derived from PPAR null mice do not produce MCP-1/JE in response to
Ox-PAPC and MM-LDL. Together, these data demonstrate a proinflammatory
role for PPAR in mediation of the activation of
endothelial cells to produce monocyte chemotactic
activity in response to oxidized phospholipids and lipoproteins.
Key Words: atherosclerosis • lipoproteins • phospholipids • interleukins • monocyte chemotactic protein-1 • endothelium
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