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Originally published In Press as doi:10.1074/jbc.M203421200 on May 20, 2002

J. Biol. Chem., Vol. 277, Issue 30, 27120-27129, July 26, 2002
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Orphan Nuclear Hormone Receptor Rev-erbalpha Regulates the Human Apolipoprotein CIII Promoter*

Hervé CosteDagger and Joan C. Rodríguez§

From GlaxoSmithKline, 25 avenue du Québec, 91951 Les Ulis cedex, France

Apolipoprotein CIII (apoCIII) plays an important role in plasma triglyceride and remnant lipoprotein metabolism. Because hypertriglyceridemia is an independent risk factor in coronary artery disease and the presence in plasma of triglyceride-rich remnant lipoproteins is correlated with atherosclerosis, considerable research efforts have been focused on the identification of factors regulating apoCIII gene expression to decrease its production. Here we report that the orphan nuclear hormone receptor Rev-erbalpha regulates the human apoCIII gene promoter. In apoCIII expressing human hepatic HepG2 cells, transfection of Rev-erbalpha specifically repressed apoCIII gene promoter activity. We determined by deletion and site-directed mutagenesis experiments that Rev-erbalpha dependent repression is mainly due to an element present in the proximal promoter of the apoCIII gene. In contrast, we found no functional Rev-erbalpha response elements in the convergently transcribed human apoAI gene or the common regulatory enhancer. The identified Rev-erbalpha response element coincides with a RORalpha 1 element, and in the present study we provide evidence that functional cross-talk between these orphan receptors modulates the apoCIII promoter. In vitro binding analysis showed that monomers of Rev-erbalpha bound this element but not another upstream RORalpha 1 response element. In addition, we showed that the closely related nuclear orphan receptor RVR also specifically repressed the human apoCIII gene. These studies underscore a novel physiological role for members of the Rev-erb family of nuclear receptors in the regulation of genes involved in triglyceride metabolism and the pathogenesis of atherosclerosis.

* This work was supported by a Marie Curie Fellowship of the European Community Program Quality of Life under contract number QLK5-CT-2000-60009.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.

Dagger To whom correspondence may be addressed. Tel.: 33-1-69-29-60-72; Fax: 33-1-69-07-48-92; E-mail: hjcc6201@gsk.com.

§ To whom correspondence may be addressed. Tel.: 33-1-69-29-61-22; Fax: 33-1-69-07-48-92; E-mail: jcr0226@gsk.com.

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