부산대학교 도서관

Abstract Atherosclerosis is a lipid disease characterized by accumulation of low density lipoprotein (LDL) in the artery wall. The transport of LDL across the endothelium of coronary artery is an initiating event of atherosclerosis, whose mechanism remains poorly understood. In the last decade, it has been shown that in caveolin-1 (Cav-1) deficient mice, LDL infiltration in aorta wall is decreased and CD36 expression in aortas is down-regulated, leading to regression of atherosclerotic lesions. In the present study, we show that native LDL endocytosis is decreased in endothelial cells deficient in Cav-1 or CD36. We demonstrate that Cav-1 and CD36 interact in caveolae-rich domains by different biochemical approaches. In addition, confocal microscopy reveals some colocalization of Cav-1 with CD36. These findings indicate that caveolae and CD36 are involved in native LDL endocytosis and suggest that CD36 might be a good candidate for the transport of native LDL across the endothelium, an early event in atherosclerosis. Highlights • Native LDL endocytosis is mediated by CD36 and Cav-1 in endothelial cells. • CD36 and Cav-1 co-immuno-precipitate in endothelial cells. • Native LDL endocytosis is decreased in Cav-1 siRNA treated endothelial cells. • Native LDL endocytosis is decreased in CD36 siRNA treated endothelial cells. [ABSTRACT FROM AUTHOR]