Journal of Southern Medical University ›› 2014, Vol. 34 ›› Issue (09): 1248-.

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Calreticulin-induced mitochondrial injury: a novel mechanism of cardiac hypertrophy

  

  • Online:2014-09-20 Published:2014-09-20

Abstract: 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.