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J. Lipid Res.
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A more recent version of this article appeared on December 1, 2002

Papers In Press, published online ahead of print October 1, 2002
J. Lipid Res., doi:10.1194/jlr.M200386-JLR200
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Submitted on September 27, 2002
Revised on October 1, 2002
Accepted on September 30, 2002

Identification of Rev-erbalpha as a physiological repressor of apolipoprotein C-III gene transcription

Eric Raspé, Helene Duez, Anethe Mansén, Coralie Fontaine, Catherine Fiévet, Jeab-Charles Fruchart, Bjorn Vennström, and Bart Staels

Département d'Athérosclérose, INSERM UR545, 59019, Lille Cedex

Corresponding Author: Helene.Duez{at}pasteur-lille.fr

Elevated serum levels of triglyceride-rich remnant lipoproteins (TRL) are a major risk factor predisposing to atherosclerosis. Apolipoprotein (apo) C-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-erbalpha specifically decreases basal and HNF-4 stimulated human apo C-III promoter activity. A Rev-erbalpha 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 apo C-III promoter. Finally, Rev-erbalpha -deficient mice displayed elevated serum and liver mRNA levels of apo C-III together with increased serum VLDL triglycerides. Taken together, our data identify Rev-erbalpha as a regulator of apo C-III gene expression, providing a novel, physiological role for this nuclear receptor in the regulation of lipid metabolism.


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