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J Biol Chem, Vol. 274, Issue 47, 33398-33402, November 19, 1999
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From the The clearance of free cholesterol from plasma
lipoproteins by tissues is of major quantitative importance, but it is
not known whether this is passive or receptor-mediated. Based on our
finding that scavenger receptor BI (SR-BI) promotes free cholesterol
(FC) exchange between high density lipoprotein (HDL) and cells, we tested whether SR-BI would effect FC movement in vivo using
[14C]FC- and [3H]cholesteryl ester
(CE)-labeled HDL in mice with increased (SR-BI transgenic (Tg)) or
decreased (SR-BI attenuated (att)) hepatic SR-BI expression. The
initial clearance of HDL FC was increased in SR-BI Tg mice by 72% and
decreased in SR-BI att mice by 53%, but was unchanged in apoA-I
knockout mice compared with wild-type mice. Transfer of FC to non-HDL
and esterification of FC were minor and could not explain differences.
The hepatic uptake of FC was increased in SR-BI Tg mice by 34% and
decreased in SR-BI att mice by 22%. CE clearance and uptake gave
similar results, but with much slower rates. The uptake of HDL FC and
CE by SR-BI Tg primary hepatocytes was increased by 2.2- and 2.6-fold
(1-h incubation), respectively, compared with control hepatocytes. In
SR-BI Tg mice, the initial biliary secretion of [14C]FC
was markedly increased, whereas increased [3H]FC appeared
after a slight delay. Thus, in the mouse, a major portion of the
clearance of HDL FC from plasma is mediated by SR-BI.
Division of Molecular Medicine,
Millennium Pharmaceuticals, Inc.,
Cambridge, Massachusetts 02139
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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