This study aims to investigate the role of calreticulin in (CRT) pressure overload induced cardiac hypertrophy. In our study, cardiac hypertrophy was induced by left ventricular pressure overload in male SD rats subjected to transverse aortic constriction (TAC) operation. Expression of gene and protein of calreticulin, markers of cardiac hypertrophy and endoplasmic reticulum stress (ERS) were measured with real-time qPCR and Western blot respectively. Meanwhile, atorvastatin (a known ERS inhibitor) and calreticulin-specific small interference ribonucleic acid (siRNA) were used to inhibit the expression of ERS and calreticulin respectively. The experimental data demonstrated that the gene and protein levels of calreticulin, hypertrophic and ERS markers were increased significantly in the heart tissues of TAC rat models after 4 weeks. Moreover, atorvastatin administration improved the cardiac function and reduced the expression of calreticulin and ERS markers in TAC rats. In addition, cultured primary neonatal rat cardiomyocytes (NCMs) were treated with norepinephrine (NE), angiotensionⅡ (AngⅡ) or isoprenaline (ISO) to induce hypertrophic phenotype and ERS. The expression of hypertrophic markers was reduced in NCMs transfected with calreticulin-siRNA. The results suggested that calreticulin might be a promising target for the treatment of cardiac hypertrophy.
