Effect of SET7/9-mediated endoplasmic reticulum stress on arsenic-induced hepatocyte apoptosis
10.3969/j.issn.1000-4718.2019.02.029
- VernacularTitle:SET7/9介导的内质网应激对砷致肝细胞凋亡的影响
- Author:
Lei TANG
1
;
Ru-Jia XIE
;
Lu ZHENG
;
Tian TIAN
;
Lei YU
;
Xiao-Xia HU
;
Shuang CAI
;
Zi-Hua MA
;
Qin YANG
;
Bing HAN
Author Information
1. 贵州医科大学病理生理学教研室
- Keywords:
SET7/9;
Endoplasmic reticulum stress;
Apoptosis;
Arsenic poisoning;
Liver injury
- From:
Chinese Journal of Pathophysiology
2019;35(2):370-373
- CountryChina
- Language:Chinese
-
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.
