on August 14, 2003
Arteriosclerosis, Thrombosis, and Vascular Biology. 2003
Published online before print August 14, 2003, doi: 10.1161/01.ATV.0000091363.28501.84
Published online before print August 14, 2003, doi: 10.1161/01.ATV.0000091363.28501.84
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Submitted on July 3, 2003
Accepted on July 28, 2003
Influence of the HDL Receptor SR-BI on Lipoprotein Metabolism and Atherosclerosis
Bernardo L. Trigatti *;
From the Department of Biochemistry (B.L.T.), McMaster University, Hamilton, Ontario, Canada; Biology Department (M.K.), Massachusetts Institute of Technology, Cambridge, Mass; and Departamento de Gastroenterología (A.R.), Facultad de Medicina, Pontificia Universidad Católica, Santiago, Chile.
* To whom correspondence should be addressed. E-mail: trigatt{at}mcmaster.ca.
Abstract--The scavenger receptor class B type I (SR-BI) was the first molecularly well-defined cell-surface HDL receptor to be described. SR-BI mediates selective HDL cholesterol uptake by formation of a productive lipoprotein/receptor complex, which requires specific structural domains and conformation states of apolipoprotein A-I present in HDL particles. SR-BI is abundantly expressed in several tissues, including the liver, where its expression is regulated by various mechanisms, including the transcriptional activity of nuclear receptors. The importance of SR-BI in overall HDL cholesterol metabolism in vivo has been definitively established by SR-BI gene manipulation in mice. These studies have shown the antiatherogenic activity of SR-BI expression in the mouse. Remarkably, SR-BI/apolipoprotein E double-knockout mice develop complex coronary artery disease, myocardial infarction, and heart failure. Additional studies should help to define the importance of SR-BI in human health and disease.
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