Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:721-727
© 2000 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Gene Transfer and Hepatic Overexpression of the HDL Receptor SR-BI Reduces Atherosclerosis in the Cholesterol-Fed LDL Receptor–Deficient Mouse
From the Department of Molecular and Cellular Engineering (K.F.K., M.H.D., J.M.G.), Department of Medicine (D.J.R.), and Institute for Human Gene Therapy (K.F.K., M.H.D., J.M.G., D.J.R.), University of Pennsylvania Health System, Philadelphia, Pa, and the Department of Biology, Massachusetts Institute of Technology, Cambridge (M.K.). K.F. Kozarsky and M.H. Donahee are now at the Department of Cardiovascular Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pa.
Correspondence to Karen Kozarsky, PhD, SmithKline Beecham, 709 Swedeland Rd, Mail Stop UW2510, King of Prussia, PA 19406. E-mail karen_f_kozarsky{at}sbphrd.com
Abstract—HDL cholesterol levels in humans are inversely correlated with the risk of atherosclerosis. The class B scavenger receptor type I (SR-BI) is the first molecularly well-defined HDL receptor, and hepatic overexpression of SR-BI in normal mice has been shown to result in decreased plasma HDL cholesterol levels. To determine whether SR-BI overexpression is proatherogenic or is protective against atherosclerosis, LDL receptor–deficient mice were placed on a high-fat/high-cholesterol diet for 2 or 12 weeks to induce atherosclerotic lesions of different stages and then were injected with a recombinant adenovirus encoding murine SR-BI. Transient hepatic overexpression of SR-BI in mice with both early and advanced lesions significantly decreased atherosclerosis. SR-BI expression was associated with markedly decreased HDL cholesterol and either unchanged or only modestly reduced non-HDL cholesterol levels; in all experiments, the mean HDL cholesterol levels were significantly correlated with atherosclerotic lesion size. These data suggest that interventions that promote HDL cholesterol transport and lower plasma HDL cholesterol levels can suppress atherosclerosis, even when initiated after significant lesion development. Thus, stimulation of hepatic SR-BI activity may provide a novel target for therapeutic intervention in atherosclerotic cardiovascular disease.
Key Words: adenovirus • HDL • receptors, lipoprotein • recombinant protein
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