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(Received for publication, June 16, 1997)
From the Scavenger receptor BI (SR-BI) binds high density
lipoproteins (HDL) with high affinity and mediates the selective uptake
of HDL cholesteryl ester. We examined the potential role of SR-BI in
mediating cellular cholesterol efflux. In Chinese hamster ovary cells
stably transfected with murine SR-BI, overexpression of SR-BI resulted
in a 3-4-fold stimulation of initial cholesterol efflux rates. Efflux
rates correlated with SR-BI expression in cells and HDL concentration
in the medium. When incubated with synthetic cholesterol-free HDL,
SR-BI-transfected cells showed ~3-fold increases in initial rates of
efflux compared with control cells, indicating that SR-BI expression
enhances net cholesterol efflux mediated by discoidal HDL. In six
different cell types, including cultured macrophages, the rate of
efflux of cholesterol mediated by HDL or serum was well correlated with
cellular SR-BI expression level. In addition, in situ
hybridization experiments revealed that SR-BI mRNA was expressed in
the thickened intima of atheromatous aorta of apolipoprotein E knockout
mice. Thus, SR-BI is an authentic HDL receptor mediating cellular
cholesterol efflux. SR-BI may facilitate the initial steps of
HDL-mediated cholesterol efflux in the arterial wall as well as later
steps of reverse cholesterol transport involving uptake of HDL
cholesterol in the liver.
Volume 272, Number 34,
Issue of August 22, 1997
pp. 20982-20985
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
COMMUNICATION:
,
,
,
Division of Molecular Medicine, Department
of Medicine, Columbia University, New York, New York 10032 and the
§ Department of Biochemistry, MCP Hahnemann School of
Medicine, Allegheny University of the Health Sciences,
Philadelphia, Pennsylvania 19129
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