Calreticulin-induced mitochondrial dysfunction is involved in cardiac hypertrophy
10.7652/jdyxb201403003
- VernacularTitle:钙网蛋白介导的线粒体功能异常参与心肌细胞肥大过程
- Author:
Hu SHAN
;
Jin WEI
;
Ming ZHANG
;
Lin LIN
;
Rui YAN
;
Rong ZHANG
- Publication Type:Journal Article
- Keywords:
calreticulin;
mitochondrial injury;
angiotensin Ⅱ;
myocardial hypertrophy
- From:Journal of Xi'an Jiaotong University(Medical Sciences)
2014;(3):295-299
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe whether calreticulin-induced mitochondrial dysfunction is involved in cardiomyocyte hypertrophy induced by angiotensin Ⅱ (AngⅡ).Methods Primary culture of neonatal rat cardiomyocytes was further confirmed by immunocytochemistry.The cardiomyocytes were randomly divided into model group,valsartan group and control group.The model group was subdivided into three groups which were separately treated with 1 0-8 mmol/L, 1 0-7 mmol/L, and 1 0-6 mmol/L Ang Ⅱ. Calreticulin expression, mitochondrial membrane potential level, enzyme activities, cell surface area and protein synthesis rate were observed.Results Cell surface area and protein synthesis rate were both increased in model groups compared with control group.Mitochondrial membrane potential level and enzyme activities were lower in model groups than in control group,while calreticulin expression was up-regulated.Pretreatment with valsartan partially reversed all the above changes.Conclusion Mitochondrial dysfunction induced by calreticulin may be an important mechanism of myocardial hypertrophy.
