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J. Biol. Chem., Vol. 279, Issue 14, 14140-14146, April 2, 2004

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Expression of Caveolin-1 Enhances Cholesterol Efflux in Hepatic Cells^*

Ying Fu, Anh Hoang, Genevieve Escher, Robert G. Parton, Zygmunt Krozowski, and Dmitri Sviridov¶

From the Wynn Domain, Baker Heart Research Institute, Melbourne, Victoria 8008 and the Institute for Molecular Bioscience, Center for Microscopy and Microanalysis, and School of Biomedical Science, University of Queensland, Brisbane, Queensland 4072, Australia

HepG2 cells were stably transfected with human caveolin-1 (HepG2/cav cells). Transfection resulted in expression of caveolin-1 mRNA, a high abundance of caveolin-1 protein, and the formation of caveolae on the plasma membrane. Cholesterol efflux from HepG2/cav cells was 280 and 45% higher than that from parent HepG2 cells when human plasma and human apoA-I, respectively, were used as acceptors. The difference in efflux was eliminated by treatment of cells with progesterone. There was no difference in cholesterol efflux to cyclodextrin. Cholesterol efflux from plasma membrane vesicles was similar for the two cell types. Transfection led to a 40% increase in the amount of plasma membrane cholesterol in cholesterol-rich domains (caveolae and/or rafts) and a 67% increase in the rate of cholesterol trafficking from intracellular compartments to these domains. Cholesterol biosynthesis in HepG2/cav cells was increased by 2-fold, and cholesterol esterification was reduced by 50% compared with parent HepG2 cells. The proliferation rate of transfected cells was significantly lower than that of non-transfected cells. Transfection did not affect expression of ABCA1 or the abundance of ABCA1 protein, but decreased secretion of apoA-I. We conclude that overexpression of caveolin-1 in hepatic cells stimulates cholesterol efflux by enhancing transfer of cholesterol to cholesterol-rich domains in the plasma membrane.

Received for publication, October 8, 2003 , and in revised form, December 23, 2003.

^* This work was supported by the National Health and Medical Research Council of Australia and by a grant from the Swiss National Foundation (to G. E.). The costs of publication of this article were defrayed in part by the payment of page charges. This 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: Baker Heart Research Inst., St. Kilda Rd. Central, P. O. Box 6492, Melbourne, Victoria 8008, Australia. Tel.: 61-3-8532-1363; Fax: 61-3-8532-1100; E-mail: Dmitri.Sviridov{at}Baker.edu.au.

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