Chieko Mineo1, Philip W Shaul. 1. Division of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA. Chieko.mineo@utsouthwestern.edu
Abstract
PURPOSE OF REVIEW: This review highlights the diverse roles of the high-affinity HDL receptor scavenger receptor class B, type I (SR-BI) in the modulation of global cholesterol homeostasis and vascular cell function, and the potential implications of these processes in atherosclerosis. RECENT FINDINGS: SR-BI in the liver plays a critical role in reverse cholesterol transport and it dramatically impacts the characteristics of the HDL particle, and through reverse cholesterol transport it promotes an antiatherogenic lipid environment in the vascular wall. SR-BI in macrophages may influence their inflammatory phenotype. In endothelial cells, SR-BI mediates HDL-induced endothelial nitric oxide synthase activation and proliferation and migration, and in platelets SR-BI may be prothrombotic in the setting of dyslipidemia. Several polymorphisms of SR-BI have been reported in humans that influence receptor expression or function. SUMMARY: In addition to regulating global lipid metabolism, SR-BI influences the functions of a variety of vascular cells relevant to atherosclerosis. Studies of SR-BI genetics in humans partially support the conclusions drawn from experimental models. However, because of the multiple functions of SR-BI, the diversity of cell types in which it is expressed, and the influence of the receptor on the characteristics of its own ligand, our understanding of the biology of the receptor is just emerging.
PURPOSE OF REVIEW: This review highlights the diverse roles of the high-affinity HDL receptor scavenger receptor class B, type I (SR-BI) in the modulation of global cholesterol homeostasis and vascular cell function, and the potential implications of these processes in atherosclerosis. RECENT FINDINGS:SR-BI in the liver plays a critical role in reverse cholesterol transport and it dramatically impacts the characteristics of the HDL particle, and through reverse cholesterol transport it promotes an antiatherogenic lipid environment in the vascular wall. SR-BI in macrophages may influence their inflammatory phenotype. In endothelial cells, SR-BI mediates HDL-induced endothelial nitric oxide synthase activation and proliferation and migration, and in platelets SR-BI may be prothrombotic in the setting of dyslipidemia. Several polymorphisms of SR-BI have been reported in humans that influence receptor expression or function. SUMMARY: In addition to regulating global lipid metabolism, SR-BI influences the functions of a variety of vascular cells relevant to atherosclerosis. Studies of SR-BI genetics in humans partially support the conclusions drawn from experimental models. However, because of the multiple functions of SR-BI, the diversity of cell types in which it is expressed, and the influence of the receptor on the characteristics of its own ligand, our understanding of the biology of the receptor is just emerging.
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