Role of calreticulin-induced mitochondrial damage in high glucose-in-duced apoptosis of myocardial cells
10.3969/j.issn.1000-4718.2015.06.002
- VernacularTitle:钙网蛋白介导线粒体损伤在高糖诱导心肌细胞凋亡中的作用
- Author:
Rui YAN
;
Hu SHAN
;
Lin LIN
;
Jiayu DIAO
;
Ming ZHANG
;
Yanhe ZHU
;
Wuhong TAN
;
Jin WEI
- Publication Type:Journal Article
- Keywords:
High glucose;
Calreticulin;
Mitochondrial injury;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2015;(6):967-972
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To observe the effect of high glucose on the protein expression of calreticulin ( CRT) and its association with cell apoptosis and mitochondrial dysfunction in the cardiomyocytes.METHODS: AC-16 cardiomyocytes were randomly divided into normal glucose group, high glucose group, high glucose+CRT siRNA group and isotonic con-trol group.The cell apoptotic rate, reactive oxygen species (ROS), mitochondrial membrane potential level, respiratory enzyme activity, and protein expression of CRT were observed.RESULTS: Compared with the cardiomyocytes in normal glucose group, the apoptotic rate and ROS production of cardiomyocytes increased in high glucose group, accompanying with the decreases in the mitochondrial membrane potential level and enzyme activitiy of the respiratory chain.The protein expression of CRT was significantly increased in high glucose group.However, compared with high glucose group, high glucose+CRT siRNA decreased the expression of CRT and attenuated the damage of mitochondria, but CRT siRNA did not reduce the ROS level in cardiomyocytes.CONCLUSION:High glucose brings about CRT over-expression to induce mito-chondrial injury, thus increasing myocardial apoptosis.
