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Originally published In Press as doi:10.1074/jbc.M011302200 on February 6, 2001

J. Biol. Chem., Vol. 276, Issue 19, 16567-16572, May 11, 2001
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Oxidized Low Density Lipoprotein Decreases Macrophage Expression of Scavenger Receptor B-I*

Jihong Han, Andrew C. Nicholson, Xiaoye Zhou, Jianwei Feng, Antonio M. Gotto Jr., and David P. HajjarDagger

From the Center of Vascular Biology, Weill Medical College of Cornell University, New York, New York 10021

Scavenger receptor class B type I (SR-BI) has recently been identified as a high density lipoprotein (HDL) receptor that mediates bidirectional flux of cholesterol across the plasma membrane. We have previously demonstrated that oxidized low density lipoprotein (OxLDL) will increase expression of another class B scavenger receptor, CD36 (Han, J., Hajjar, D. P., Febbraio, M., and Nicholson, A. C. (1997) J. Biol. Chem. 272, 21654-21659). In studies reported herein, we evaluated the effects of OxLDL on expression of SR-BI in macrophages to determine how exposure to this modified lipoprotein could alter SR-BI expression and cellular lipid flux. OxLDL decreased SR-BI expression in a dose- and time-dependent manner. Incubation with OxLDL had no effect on the membrane distribution of SB-BI, and it decreased expression of both cytosolic and membrane protein. Consistent with its effect on SR-BI protein expression, OxLDL decreased SR-BI mRNA in a dose-dependent manner. The ability of OxLDL to decrease SR-BI expression was dependent on the degree of LDL oxidation. OxLDL decreased both [14C]cholesteryl oleate/HDL uptake and efflux of [14C]cholesterol to HDL in a time-dependent manner. Incubation of macrophages with 7-ketocholesterol, but not free cholesterol, also inhibited expression of SR-BI. Finally, we demonstrate that the effect of OxLDL on SR-BI is dependent on the differentiation state of the monocyte/macrophage. These results imply that in addition to its effect in inducing foam cell formation in macrophages through increased uptake of oxidized lipids, OxLDL may also enhance foam cell formation by altering SR-BI-mediated lipid flux across the cell membrane.

* This work was supported by National Institutes of Health Specialized Center for Research in Atherosclerosis Grant in Molecular Medicine and Atherosclerosis P50-HL56987 (to A. C. N. and D. P. H.) and the Abercrombie Foundation (to A. M. G.).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 should be addressed: Dept. of Pathology and Center of Vascular Biology, Weill Medical College of Cornell University, 1300 York Ave., New York, NY 10021.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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