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

TAO Yong Kang YU Pu Lin BAI Yong Ping YAN Sheng Tao ZHAO Shui Ping ZHANG Guo Qiang

TAO Yong Kang, YU Pu Lin, BAI Yong Ping, YAN Sheng Tao, ZHAO Shui Ping, ZHANG Guo Qiang. Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis[J]. Biomedical and Environmental Sciences, 2016, 29(12): 868-876. doi: 10.3967/bes2016.116
Citation: TAO Yong Kang, YU Pu Lin, BAI Yong Ping, YAN Sheng Tao, ZHAO Shui Ping, ZHANG Guo Qiang. Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis[J]. Biomedical and Environmental Sciences, 2016, 29(12): 868-876. doi: 10.3967/bes2016.116

doi: 10.3967/bes2016.116
基金项目: State Key Clinical Specialty Construction Project, China

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

Funds: State Key Clinical Specialty Construction Project, China
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  • 刊出日期:  2016-12-20

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

doi: 10.3967/bes2016.116
    基金项目:  State Key Clinical Specialty Construction Project, China

摘要: Objective PERK/eIF2α/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/eIF2α/CHOP signaling pathway in vascular endothelial cells. Methods The effects of ox-LDL on PERK and p-eIF2α protein expression of primary human umbilical vein endothelial cells (HUVECs) were investigated by Western blot analysis. PERK gene silencing and selective eIF2α phosphatase inhibitor, salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis, caspase-3 activity, and CHOP mRNA level. Results Ox-LDL treatment significantly increased the expression of PERK, PERK-mediated inactivation of eIF2α 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 shRNA or by selective eIF2α phosphatase inhibitor, salubrinal. Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/eIF2α/CHOP ER-stress pathway. It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis.

English Abstract

TAO Yong Kang, YU Pu Lin, BAI Yong Ping, YAN Sheng Tao, ZHAO Shui Ping, ZHANG Guo Qiang. Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis[J]. Biomedical and Environmental Sciences, 2016, 29(12): 868-876. doi: 10.3967/bes2016.116
Citation: TAO Yong Kang, YU Pu Lin, BAI Yong Ping, YAN Sheng Tao, ZHAO Shui Ping, ZHANG Guo Qiang. Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis[J]. Biomedical and Environmental Sciences, 2016, 29(12): 868-876. doi: 10.3967/bes2016.116

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