Oxidized LDL activates fas-mediated endothelial cell apoptosis.
Oxidized LDL activates fas-mediated endothelial cell apoptosis.
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DOI：
10.1172/jci3531
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发表时间：
1998-11
期刊：
影响因子：
--
通讯作者：
M. Sata;K. Walsh
中科院分区：
文献类型：
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作者：
M. Sata;K. Walsh
氧化低密度脂蛋白 (OxLDL) 会促进脉管系统中的慢性炎症反应，从而导致动脉粥样硬化斑块。 Fas 配体 (FasL) 在血管内皮上自然表达，当表达 Fas 的免疫细胞进入血管壁时，它可以诱导它们凋亡。尽管血管内皮细胞通常能够抵抗 Fas 介导的细胞死亡，但 OxLDL 可以通过 Fas L 中和抗体抑制的过程诱导培养的内皮细胞和动脉外植体内皮细胞凋亡。与野生型小鼠相比，gld (FasL-/-) 和 lpr (Fas-/-) 小鼠的主动脉内皮细胞中 OxLDL 诱导的细胞死亡也减少。 OxLDL 的作用是使内皮细胞对来自 Fas 受体的死亡信号敏感。因此，OxLDL 促进 Fas 介导的内皮细胞自杀的能力可能是导致其致动脉粥样硬化的一个特征。
Oxidized low density lipoproteins (OxLDL) promote chronic inflammatory responses in the vasculature that give rise to atherosclerotic plaques. Fas ligand (FasL) is naturally expressed on the vascular endothelium where it can induce apoptosis in Fas-expressing immune cells as they enter the vessel wall. Although vascular endothelial cells are normally resistant to Fas-mediated cell death, OxLDL were shown to induce apoptosis in cultured endothelial cells and endothelium of arterial explants by a process that could be inhibited with Fas L neutralizing antibodies. OxLDL-induced cell death was also reduced in the aortic endothelium cultured from gld (FasL-/-) and lpr (Fas-/-) mice as compared with wild-type mice. OxLDL acted by sensitizing endothelial cells to death signals from the Fas receptor. Thus, the ability of OxLDL to promote Fas-mediated endothelial cell suicide may be a feature that contributes to their atherogenicity.