Effect of SET7/9-mediated endoplasmic reticulum stress on arsenic-induced hepatocyte apoptosis |
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Authors: | TANG Lei XIE Ru-jia ZHENG Lu TIAN Tian YU Lei HU Xiao-xia CAI Shuang MA Zi-hua YANG Qin HAN Bing |
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Affiliation: | 1. Department of Pathophysiology, Key Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases in Guizhou Province, Guizhou Medical University, Guiyang 550000, China;2. Department of Physiology, Guizhou Medical University, Guiyang 550000, China |
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Abstract: | AIM:To investigate the effect of SET7/9 (SET domain containing 7/9)-mediated endoplasmic reticulum stress (ERS) on protein kinase R-like endoplasmic reticulum kinase (PERK) signaling pathway, and to explore the mechanisms of arsenic-induced hepatocyte apoptosis. METHODS:Human liver LO2 cells were divided into control group, arsenic poisoning model group, negative transfection group and SET7/9 siRNA transfection group. The apoptosis of the LO2 cells in each group was analyzed by flow cytometry. The protein levels of SET7/9, glucose-regulated protein 78 (GRP78), PERK and p-PERK in the LO2 cells of each group were observed by Western blot. RESULTS:Inhibition of SET7/9 expression reduced the apoptotic rate of arsenic-induced LO2 cells. Arsenic exposure increased the expression of SET7/9 in the LO2 cells. Arsenic exposure increased the protein levels of GRP78 and p-PERK in the LO2 cells, but decreased the protein levels of GRP78 and p-PERK after transfection with SET7/9 siRNA (P<0.05). CONCLUSION:Arsenic exposure induces hepatocyte apoptosis by increasing SET7/9 to activate ERS by PERK signaling pathway. |
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Keywords: | SET7/9 Endoplasmic reticulum stress Apoptosis Arsenic poisoning Liver injury |
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