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J. Biol. Chem., Vol. 277, Issue 30, 27120-27129, July 26, 2002
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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-erb
Orphan Nuclear Hormone Receptor Rev-erb
Regulates
the Human Apolipoprotein CIII Promoter*
and
regulates the human apoCIII gene promoter. In
apoCIII expressing human hepatic HepG2 cells, transfection of
Rev-erb specifically repressed apoCIII gene promoter activity. We
determined by deletion and site-directed mutagenesis experiments that
Rev-erb dependent repression is mainly due to an element present in
the proximal promoter of the apoCIII gene. In contrast, we found no
functional Rev-erb response elements in the convergently transcribed
human apoAI gene or the common regulatory enhancer. The identified
Rev-erb response element coincides with a ROR1 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-erb bound
this element but not another upstream ROR1 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.
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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