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J Biol Chem, Vol. 274, Issue 4, 2366-2371, January 22, 1999
From the Division of Molecular Medicine, Department of Medicine,
Columbia University, New York, New York 10032
Scavenger receptor type B class I (SR-BI),
initially identified as a receptor that recognizes low density
lipoprotein (LDL), was recently shown to mediate the selective uptake
of high density lipoprotein (HDL) cholesteryl esters in liver and
steroidogenic tissues. To evaluate effects on atherosclerosis,
transgenic mice with liver-specific overexpression of SR-BI (SR-BI Tg
mice) have been crossed onto LDL receptor-deficient backgrounds. To
induce atherosclerosis in a setting of moderate hypercholesterolemia, heterozygous LDL receptor-deficient mice (LDLR1) were fed a high fat/cholesterol/bile salt diet, and homozygous LDL receptor knock-outs (LDLR0) were fed a high fat/cholesterol diet. LDLR1/SR-BI Tg mice showed decreases in VLDL, LDL, and HDL cholesterol and a significant 80% decrease in mean lesion area in the aortic root compared with LDLR1 mice (female LDLR1 74, 120 µm2
versus LDLR1/SR-BI Tg 12, 667 µm2; male 25, 747 µm2 versus 5, 448 µm2,
respectively). LDLR0/SR-BI Tg mice showed decreased LDL and HDL
cholesterol but increased VLDL cholesterol and no significant difference in extent of atherosclerosis compared with LDLR0 mice. Combined data analysis showed a strong correlation between
atherosclerotic lesion area and the VLDL+LDL cholesterol level but no
correlation with HDL level. These studies demonstrate a strong
anti-atherogenic potential of hepatic SR-BI overexpression. In mice
with marked overexpression of SR-BI, the protective effect appears to
be primarily related to the lowering of VLDL and LDL cholesterol levels.
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