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Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis

查看全文 作　　者：TAO Yong [1]Kang;YU Pu [2]Lin;BAI Yong [3]Ping;YAN Sheng [1]Tao;ZHAO Shui [4]Ping;ZHANG Guo [1]Qiang 高影响力作者 机构地区：[1]Departments of Emergency,China-Japan Friendship Hospital,Beijing 100029,China;[2]Beijing Institution of Geriatrics,Beijing Hospital,Beijing 100730,China;[3]Department of Geriatric Medicine,Xiangya Hospital,Central South University,Changsha 410008,Hunan,China;[4]Department of Cardiology,The Second Xiangya Hospital,Central South University,Changsha 410011,Hunan,China高影响力机构 出　　处：《Biomedical and Environmental Sciences》索引2016年第29卷第12期,共9页高影响力期刊 基　　金：State Key Clinical Specialty Construction Project,China 摘　　要：Objective PERK/eI F2α/CHOP is a major signaling pathway mediating endoplasmic reticulum(ER) stress related with atherosclerosis.Oxidized LDL(ox-LDL) also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis.The present study was conducted to explore the regulatory effect of ox-LDL on PERK/e IF2α/CHOP signaling pathway in vascular endothelial cells.Methods The effects of ox-LDL on PERK and p-e IF2α protein expression of primary human umbilical vein endothelial cells(HUVECs) were investigated by Western blot analysis.PERK gene silencing and selective eI F2α phosphatase inhibitor,salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis,caspase-3 activity,and CHOP mR NA level.Results Ox-LDL treatment significantly increased the expression of PERK,PERK-mediated inactivation of e IF2α phosphorylation,and the expression of CHOP,as well as the caspase-3 activity and apoptosis.The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral sh RNA or by selective eI F2α phosphatase inhibitor,salubrinal.Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/eI F2α/CHOP ER-stress pathway.It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis. 关 键 词：PERK EIF2Α CHOP Endoplasmic reticulum stress Oxidized low-density lipoprotein Endothelial cell Apoptosis ATHEROSCLEROSIS Caspase-3
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