Homocysteine mediates cardiomyocyte apoptosis by phosphorylating PERK and activating CHOP-ERO1α pathway
10.3969/j.issn.1671-8348.2018.05.003
- VernacularTitle:同型半胱氨酸经PERK磷酸化激活CHOP-ERO1α通路介导心肌细胞凋亡的研究
- Author:
Hailin DU
1
;
Shaobing YANG
;
Guangzhi CONG
;
Kai WANG
;
Shaobin JIA
Author Information
1. 宁夏医科大学临床医学院
- Keywords:
homocysteine;
CCAAT-enhancer-binding protein homologous protein;
endoplasmic reticulum oxidoreductin-α;
myocytes,cardiac;
apoptosis
- From:
Chongqing Medicine
2018;47(5):584-587
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of homocysteine(Hcy) on myocardial injury and its possible mechanisms.Methods The selected H9C2 cardiomyocytes were intervened with various concentrations of Hcy and 4-phenyl butyric acid(4-PBA).The H9C2 cells were divided into the control group,H400 group and H400P2 group.The control group used the common medium,the H400 group was added with 400 μmol/L Hcy,the H400P2 group was added with 2 mmol/L 4-PBBA on the basis of H400 group.The cell livability was detected by using cell counting kit-8 (CCK-8).Apoptosis was evaluated by using the terminal deoxynucleotidyl transferase mediated nick-end labelling(TUNEL) staining.The ERO1α expression was determined by using immunocytochemistry,and the protein expression difference was determined by using Western blot.Results The injury of Hey on H9C2 cardiomyocytes showed a concentration-dependent manner(F=2 039.958,P＜0.01).Compared with the control group,the apoptosis percentages and expression levels of PERK,p-PERK,CHOP and ERO1α in the H400 group were increased(P＜0.01);while which in the H400P2 group were decreased,the difference was statistically significant(P＜0.05).Conclusion Hcy mediates myocardial apoptosis through endoplasmic reticulum stress mechanism.
