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首页> 外文期刊>Journal of Cellular Physiology >Ox‐LDL induces endothelial cell apoptosis and macrophage migration by regulating caveolin‐1 phosphorylation
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Ox‐LDL induces endothelial cell apoptosis and macrophage migration by regulating caveolin‐1 phosphorylation

机译:牛的低密度脂蛋白诱导内皮细胞凋亡和通过调节巨噬细胞迁移窖蛋白量1磷酸化

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摘要

Oxidative low‐density lipoprotein (ox‐LDL) is a risk factor for atherosclerosis. Ox‐LDL leads to endothelial injury in the initial stage of atherosclerosis. In this study, we investigated the role of ox‐LDL in endothelial injury and macrophage recruitment. We demonstrated that ox‐LDL promoted a dose‐dependent phosphorylation of caveolin‐1 in human umbilical vein endothelial cells. Phosphorylated caveolin‐1 increased ox‐LDL uptake. Intracellular accumulation of ox‐LDL induced NF‐κB p65 phosphorylation, promoted HMGB1 translocation from nucleus to cytoplasm and cytochrome C release from mitochondria to cytoplasm, and activated caspase 3, resulting in cell apoptosis. NF‐κB activation also facilitated cavolin‐1 phosphorylation and HMGB1 expression. In addition, caveolin‐1 phosphorylation favored HMGB1 release and nuclear translocation of EGR1. Nuclear translocation of EGR1 contributed to cytoplasmic translocation of HMGB1. The extracellular HMGB1 induced the migration of PMBC‐derived macrophages toward HUVECs in a TLR4‐dependent manner. Our results suggested that ox‐LDL promoted HUVECs apoptosis and macrophage recruitment by regulating caveolin‐1 phosphorylation.
机译:氧化低密度脂蛋白应承担(牛所致的低密度脂蛋白)是一个动脉粥样硬化的危险因素。内皮损伤的初始阶段动脉粥样硬化。牛的角色在内皮损伤和低密度脂蛋白巨噬细胞招聘。牛LDL提拔一个剂量依赖的磷酸化量窖蛋白1在人类脐静脉内皮细胞。吸收。诱导NF必经κB p65磷酸化,提升HMGB1从细胞质和核易位线粒体细胞色素C的释放细胞质,激活半胱天冬酶3,导致细胞凋亡。cavolin 1磷酸化和HMGB1表达。此外,量1窖蛋白磷酸化青睐HMGB1 EGR1释放和核易位。核易位EGR1导致细胞质HMGB1的易位。细胞外HMGB1诱导的迁移PMBC派生向HUVECs在巨噬细胞TLR4依赖的方式。牛的低密度脂蛋白促进HUVECs凋亡和巨噬细胞招聘通过调节窖蛋白量1磷酸化。

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