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Originally published In Press as doi:10.1074/jbc.M203436200 on July 9, 2002

J. Biol. Chem., Vol. 277, Issue 37, 34176-34181, September 13, 2002
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Constitutive Activation of Peroxisome Proliferator-activated Receptor-gamma Suppresses Pro-inflammatory Adhesion Molecules in Human Vascular Endothelial Cells*

Nanping WangDagger §, Lynne VernaDagger , Neng-Guin Chen, Jasmine Chen, Hongling LiDagger , Barry Marc Forman||, and Michael B. StemermanDagger

From the Dagger  Division of Biomedical Sciences, University of California, Riverside, California 92521, the  Division of Molecular Medicine and The Gonda Diabetes and Genetic Research Center, and the || Department of Diabetes, Endocrinology, and Metabolism, The City of Hope National Medical Center, Beckman Research Institute, Duarte, California 91010

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma ) is a ligand-activated nuclear receptor that has an essential role in adipogenesis and glucose homeostasis. PPAR-gamma is expressed in vascular tissues including endothelial cells (ECs). PPAR-gamma activity can be regulated by many pathophysiological and pharmacological agonists. However, the role of PPAR-gamma activation in ECs remains unclear. In this study, we examined the effect of the constitutive activation of PPAR-gamma on the phenotypic modulation of ECs. Adenovirus-mediated expression of a constitutively active mutant of PPAR-gamma resulted in significant ligand-independent activation of PPAR-gamma and specific induction of the PPAR-gamma target genes. However, PPAR-gamma activation significantly suppressed the expression of vascular adhesion molecules in ECs and the ensuing leukocyte recruitment. Furthermore, constitutive activation of PPAR-gamma resulted in simultaneous repression of AP-1 and NF-kappa B activity, which suggests that PPAR-gamma may reduce pro-inflammatory phenotypes via, at least in part, suppression of the AP-1 and NF-kappa B pathways. Therefore, using a gain-of-function approach, our study provides novel evidence showing that constitutive activation of PPAR-gamma is sufficient to prevent ECs from converting into a pro-inflammatory phenotype. These results also suggest that, in addition to pharmacological agonists, the genetic modification of the PPAR-gamma activity in ECs may be a potential approach for therapeutic intervention in various inflammatory disorders.

* This work was supported in part by Research Grants 0130276N from the American Heart Association (to N. W.) and HL33742-15A1 from the National Institutes of Health (to M. B. S.).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. Tel.: 909-77-4553; Fax: 909-787-5504; E-mail: nanping.wang@ucr.edu.

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