Vitamin E reduces the uptake of oxidized LDL by inhibiting CD36 scavenger receptor expression in cultured aortic smooth muscle cells

Article

关键词: PROTEIN-KINASE-C;    LOW-DENSITY LIPOPROTEINS;    TUMOR NECROSIS FACTOR;    D-ALPHA-TOCOPHEROL;    ATHEROSCLEROSIS;    MACROPHAGES;    DIFFERENTIATION;    IDENTIFICATION;    PROLIFERATION;    RESISTANCE;   

DOI  :  10.1161/01.CIR.102.1.82

来源: SCIE

【 摘 要 】

Background-Vitamin E is well known as an antioxidant, and numerous studies suggest that it has a preventive role in atherosclerosis. although the mechanism of action still remains unclear. Methods and Results-The original aim of this study was to establish whether alpha-tocopherol (the most active form of vitamin E) acts at the earliest events on the cascade of atherosclerosis progression, that of oxidized LDL (oxLDL) uptake and foam-cell formation. We show here that the CD36 scavenger receptor (a specific receptor for oxLDL) is expressed in cultured human aortic smooth muscle cells (SMCs). Treatment of SMCs and HL-60 macrophages with alpha-tocopherol (50 mu mol/L, a physiological concentration) downregulates CD36 expression by reducing its promoter activity. Furthermore, we find that alpha-tocopherol treatment of SMCs leads to a reduction of oxLDL uptake. Conclusions-This study indicates that CD36 is expressed in cultured human SMCs. In these cells, CD36 transports oxLDL into the cytosol. alpha-Tocopherol inhibits oxLDL uptake by a mechanism involving downregulation of CD36 mRNA and protein expression. Therefore, the beneficial effect of alpha-tocopherol against atherosclerosis can be explained, at least in part, by its effect of lowering the uptake of oxidized lipoproteins, with consequent reduction of foam cell formation.

【 授权许可】

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