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高密度脂蛋白对氧化型低密度脂蛋白诱导的U937/内皮细胞相互作用的保护作用。

The protective role of high-density lipoprotein on oxidized-low-density-lipoprotein-induced U937/endothelial cell interactions.

作者信息

Maier J A, Barenghi L, Pagani F, Bradamante S, Comi P, Ragnotti G

机构信息

Department of Biomedical Sciences, Technologies-Ospedale San Raffaele, Milan, Italy.

出版信息

Eur J Biochem. 1994 Apr 1;221(1):35-41. doi: 10.1111/j.1432-1033.1994.tb18712.x.

Abstract

The adherence of monocytes to the endothelium is an early event in atherogenesis. We have investigated this process by examining whether native and oxidized low-density and high-density lipoproteins could modulate this process. Only oxidized low-density lipoprotein caused a significant dose-dependent and time-dependent increase in U937 monocyte-like cell line binding to human endothelial cells, by a process which required de novo protein synthesis. Interestingly, E-selectin, intercellular adhesion molecule-1, vascular cell-adhesion molecule or P-selectin induction was not apparent in this system suggesting the presence of an alternative system for the interaction of endothelial cells with monocyte-like cells in response to oxidized low-density lipoprotein. High-density lipoprotein completely suppressed oxidized low-density-lipoprotein-induced adhesion of U937 cells to the endothelial monolayer, while oxidized high-density lipoprotein did not. These data suggest that the balance between native and oxidized lipoproteins may play a role in the formation of the atherosclerotic lesion by modulating monocyte endothelial interactions.

摘要

单核细胞与内皮细胞的黏附是动脉粥样硬化形成过程中的早期事件。我们通过研究天然和氧化的低密度脂蛋白及高密度脂蛋白是否能调节这一过程来对该过程进行了调查。只有氧化型低密度脂蛋白通过一个需要从头合成蛋白质的过程,导致U937单核细胞样细胞系与人类内皮细胞的结合出现显著的剂量依赖性和时间依赖性增加。有趣的是,在该系统中未观察到E-选择素、细胞间黏附分子-1、血管细胞黏附分子或P-选择素的诱导表达,这表明存在一种替代系统,用于内皮细胞与单核细胞样细胞在氧化型低密度脂蛋白作用下的相互作用。高密度脂蛋白完全抑制了氧化型低密度脂蛋白诱导的U937细胞与内皮细胞单层的黏附,而氧化型高密度脂蛋白则没有。这些数据表明,天然脂蛋白和氧化脂蛋白之间的平衡可能通过调节单核细胞与内皮细胞的相互作用在动脉粥样硬化病变的形成中发挥作用。

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