[钙网蛋白诱导的线粒体损伤：心脏肥大的一种新机制]
[Calreticulin-induced mitochondrial injury: a novel mechanism of cardiac hypertrophy].
作者信息
Shan Hu, Wei Jin, Zhang Ming, Yan Rui, Lin Lin, Zhang Rong, Zhu Yanhe, Tan Wuhong
机构信息
Department of Cardiology, Second Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an 710004, China. E-mail:
出版信息
Nan Fang Yi Ke Da Xue Xue Bao. 2014 Aug;34(9):1248-53.
OBJECTIVE
To observe the effect of angiotensin II (Ang II) on calreticulin (CRT) expression and its association with mitochondrial dysfunction in cardiomyocytes.
METHODS
Primary neonatal rat cardiomyocytes were randomly divided into CRT siRNA group, control siRNA group, control group, Ang II+ CRT siRNA group, Ang II+ control siRNA group and Ang II group. The cell surface area, protein synthesis rate, mitochondrial membrane potential level, enzyme activities, and CRT expression were observed.
RESULTS
Compared with those in the control group, the cell surface area and protein synthesis rate were both increased and mitochondrial membrane potential level and enzyme activities decreased in Ang II groups. CRT expression was significantly down-regulated in Ang II+ CRT siRNA group with increased cell surface area, protein synthesis rate, mitochondrial membrane potential level and enzyme activities as compared with those in Ang II+ control siRNA group.
CONCLUSION
Ang II up-regulates CRT expression to induce mitochondrial injury, which may be an important mechanism of myocardial hypertrophy.
目的
观察血管紧张素II（Ang II）对心肌细胞中钙网蛋白（CRT）表达的影响及其与线粒体功能障碍的关系。
方法
将原代新生大鼠心肌细胞随机分为CRT siRNA组、对照siRNA组、对照组、Ang II + CRT siRNA组、Ang II +对照siRNA组和Ang II组。观察细胞表面积、蛋白质合成率、线粒体膜电位水平、酶活性及CRT表达。
结果
与对照组相比，Ang II组细胞表面积和蛋白质合成率均增加，线粒体膜电位水平和酶活性降低。Ang II + CRT siRNA组CRT表达明显下调，与Ang II +对照siRNA组相比，细胞表面积、蛋白质合成率、线粒体膜电位水平和酶活性增加。
结论
Ang II上调CRT表达以诱导线粒体损伤，这可能是心肌肥大的重要机制。
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