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Originally published In Press as doi:10.1194/jlr.M200386-JLR200 on October 1, 2002

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Journal of Lipid Research, Vol. 43, 2172-2179, December 2002
Copyright © 2002 by Lipid Research, Inc.

Identification of Rev-erb{alpha} as a physiological repressor of apoC-III gene transcription1

Eric Raspé2,*,{dagger}, Hélène Duez2,*, Anethe Mansén§, Coralie Fontaine*, Catherine Fiévet*, Jean-Charles Fruchart*,**, Bjorn Vennström§ and Bart Staels3,*,**

* UR 545 INSERM, Institut Pasteur de Lille, 1 rue Calmette, 59019 Lille, France
{dagger} Groupe Merck, Centre de Recherche et Développement, 115 av. Lacassagne, 69003 Lyon, France
§ Karolinska Institute, Department of Cellular and Molecular Biology, S-17177 Stockholm, Sweden
** Faculté de Pharmacie, Université de Lille II, 59006 Lille, France

3 To whom correspondence should be addressed. e-mail: bart.staels{at}pasteur-lille.fr

Elevated serum levels of triglyceride-rich remnant lipoproteins (TRL) are a major risk factor predisposing a subject to atherosclerosis. Apolipoprotein C-III (apoC-III) is a major constituent of TRL that impedes triglyceride hydrolysis and remnant clearance and, as such, may exert pro-atherogenic activities. In the present study, transient cotransfection experiments in rat hepatocytes in primary culture and rabbit kidney RK13 cells demonstrated that overexpression of Rev-erb{alpha} specifically decreases basal and HNF-4 stimulated human apoC-III promoter activity. A Rev-erb{alpha} response element was mapped by promoter deletion, mutation analysis, and gel-shift experiments to a AGGTCA half-site located at position -23/-18 (downstream of the TATA box) in the apoC-III promoter. Finally, Rev-erb{alpha}-deficient mice displayed elevated serum and liver mRNA levels of apoC-III together with increased serum VLDL triglycerides.

Taken together, our data identify Rev-erb{alpha} as a regulator of apoC-III gene expression, providing a novel, physiological role for this nuclear receptor in the regulation of lipid metabolism.

Supplementary key words apolipoprotein C-III • triglycerides • nuclear receptors


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