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血小板介导的胆固醇在培养的主动脉平滑肌细胞中的积累。

Platelet-mediated cholesterol accumulation in cultured aortic smooth muscle cells.

作者信息

Kruth H S

出版信息

Science. 1985 Mar 8;227(4691):1243-5. doi: 10.1126/science.3975612.

Abstract

Cholesterol accumulates within smooth muscle cells and macrophages in atherosclerotic lesions, thereby contributing to the progressive enlargement of these lesions. The mechanism of this cellular accumulation of cholesterol is not known. The possibility that platelets may have a role in the cellular cholesterol accumulation that occurs during atherogenesis was investigated. Incubation of thrombin-activated washed rat platelets (or platelet-free supernatants prepared from thrombin-activated platelets) with cultured rat aortic smooth muscle cells induced cholesteryl ester lipid droplet accumulation within the smooth muscle cells. No cholesteryl ester lipid droplets accumulated when smooth muscle cells were incubated with unactivated platelets. Smooth muscle cell lipid droplet accumulation occurred in the absence of serum lipoproteins and was not inhibited by mevinolin, a drug that blocks cholesterol synthesis. These findings suggest that activated platelets may release cholesterol, which can be accumulated by cells and stored as lipid droplets.

摘要

胆固醇在动脉粥样硬化病变的平滑肌细胞和巨噬细胞内蓄积,从而促使这些病变逐渐扩大。胆固醇这种细胞内蓄积的机制尚不清楚。研究了血小板在动脉粥样硬化形成过程中细胞胆固醇蓄积方面可能发挥的作用。用凝血酶激活的洗涤大鼠血小板(或由凝血酶激活的血小板制备的无血小板上清液)与培养的大鼠主动脉平滑肌细胞一起孵育,可诱导平滑肌细胞内胆固醇酯脂质小滴的蓄积。当平滑肌细胞与未激活的血小板一起孵育时,未出现胆固醇酯脂质小滴的蓄积。平滑肌细胞脂质小滴的蓄积在无血清脂蛋白的情况下发生,且不受洛伐他汀(一种阻断胆固醇合成的药物)的抑制。这些发现表明,激活的血小板可能释放胆固醇,胆固醇可被细胞蓄积并储存为脂质小滴。

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