钙网蛋白介导的线粒体功能异常参与心肌细胞肥大过程  

Calreticulin-induced mitochondrial dysfunction is involved in cardiac hypertrophy

作　　者：单虎[1] 魏瑾[1] 张明[1] 林琳[1] 闫蕊[1] 张蓉[1] 

机构地区：[1]西安交通大学医学院第二附属医院心内科,陕西西安710004

出　　处：《西安交通大学学报（医学版）》2014年第3期295-299,共5页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.81170209;30771862)~~

摘　　要：目的观察钙网蛋白(CRT)介导的线粒体功能异常是否参与血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥大过程。方法原代分离培养大乳鼠心肌细胞并以免疫细胞化学法鉴定其纯度,将同期培养的心肌细胞随机分为模型组、缬沙坦组和对照组,模型组共3组,分别以10-8 mmol/L、10-7 mmol/L、10-6 mmol/L AngⅡ干预。分别测定各组钙网蛋白(CRT)表达水平、线粒体膜电位、线粒体呼吸链酶活性、细胞表面积及蛋白质合成速率的变化。结果模型组细胞表面积及蛋白质合成速率明显升高,线粒体膜电位及呼吸链酶活性降低,同时CRT表达升高。而缬沙坦组心肌细胞肥大不明显,线粒体膜电位、呼吸链酶活性降低和CRT表达上调得到部分逆转。结论在AngⅡ刺激下,CRT表达升高所诱导的线粒体功能异常可能是心肌肥大的重要机制之一。Objective To observe whether calreticulin-induced mitochondrial dysfunction is involved in cardiomyocyte hypertrophy induced by angiotensin Ⅱ （Ang Ⅱ ）. 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 10^-8 mmol/L, 10^- 7 mmol/L, and 10^-6 mmol/L AngⅡ. 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. Gonclusion Mitochondrial dysfunction induced by calreticulin may be an important mechanism of myocardial hypertrophy.

关 键 词：钙网蛋白 线粒体损伤 血管紧张素Ⅱ 心肌肥大 

分 类 号：R541.3[医药卫生—心血管疾病]