低密度脂蛋白和高密度脂蛋白对牛主动脉内皮细胞中磷酸肌醇水解的影响。

The effects of low density lipoprotein and high density lipoprotein on phosphoinositide hydrolysis in bovine aortic endothelial cells.

作者信息

Myers D E, Fidge N H, Stanton H, Larkins R G

机构信息

Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Victoria, Australia.

出版信息

Atherosclerosis. 1992 Jan;92(1):9-16. doi: 10.1016/0021-9150(92)90004-z.

DOI:10.1016/0021-9150(92)90004-z

PMID:1315550

Abstract

Low density lipoprotein (LDL) and high density lipoprotein (HDL3) were tested for their ability to induce inositol phospholipid turnover and inositol phosphate production in bovine aortic endothelial cells (BAEC). The production of inositol phosphates following hydrolysis of the phosphoinositides was demonstrated by two methods; release of [3H]inositol phosphates after labelling with [3H]myo-inositol and by a direct binding assay for inositol 1,4,5-trisphosphate (InsP3). Acute exposure to LDL induced InsP3 release at low concentrations of the lipoprotein within the physiological range of LDL in tissues. HDL3 did not cause any release of the inositol phosphates. Pre-incubation of BAEC with HDL3 suppressed bradykinin- and LDL-induced inositol phosphate production in BAEC in a concentration-dependent manner. It is concluded that LDL acutely stimulates phosphoinositide breakdown and that pre-incubation of cells with HDL3 inhibits this effect. The mechanism responsible for these effects remains to be elucidated.

摘要

检测了低密度脂蛋白（LDL）和高密度脂蛋白（HDL3）在牛主动脉内皮细胞（BAEC）中诱导肌醇磷脂周转和肌醇磷酸生成的能力。通过两种方法证明了磷酸肌醇水解后肌醇磷酸的生成；用[3H]肌醇标记后[3H]肌醇磷酸的释放以及通过对肌醇1,4,5-三磷酸（InsP3）的直接结合测定。在组织中LDL的生理范围内，低浓度脂蛋白急性暴露于LDL会诱导InsP3释放。HDL3不会引起肌醇磷酸的任何释放。用HDL3对BAEC进行预孵育以浓度依赖的方式抑制了缓激肽和LDL诱导的BAEC中肌醇磷酸的生成。得出的结论是，LDL急性刺激磷酸肌醇分解，并且用HDL3对细胞进行预孵育会抑制这种作用。造成这些影响的机制仍有待阐明。