Silencing calreticulin gene might protect cardiomyocytes from angiotensin II-induced apoptosis

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Calreticulin (CRT), as a chaperone, contributes to protein folding and quality control cycle. CRT is an important factor regulating Ca2+ that participates in cell apoptosis. However, the function of CRT in the heart is still controversial. Therefore, we aimed to investigate the potential role of CRT in angiotensin II-induced cardiomyocytes apoptosis.

Main methods

Primary cultured neonatal cardiomyocytes were stimulated with angiotensin II to induce the apoptosis. Expression of CRT and endoplasmic reticulum (ER) stress associated protein was detected by western blotting after angiotensin II stimulation for 24 h. The reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) were also detected. Additionally, the function of CRT on cardiomyocytes apoptosis and ER stress/unfolded protein response signaling pathway was investigated by transfecting specific CRT-targeting siRNA.

Key findings

Cardiomyocytes apoptosis was induced by angiotensin II. The protein level of CRT was elevated after angiotensin -II stimulation for 24 h. Additionally, the protein levels of GRP78, ATF4, C-ATF6, CHOP and the ROS production were elevated, but the Bcl-2 expression and the level of MMP were down-regulated. After silencing CRT gene in the process of angiotensin II-induced cardiomyocytes apoptosis, cardiomyocytes apoptosis rate decreased, meanwhile the protein expression of CRT, GRP78, ATF4, C-ATF6 and CHOP were down-regulated. However, the Bcl-2 expression was up-regulated, and the increase of ROS and the loss of MMP were alleviated.


Our study demonstrated that CRT might protect cardiomyocytes from apoptosis induced by angiotensin II, in which ER stress and mitochondria function were identified as possible underlying molecular bases.

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