Endogenous sestrin2 is involved in inhibiting endoplasmic reticulum stress mediated apoptosis after myocardial infarction

  AIM  To reveal the change and role of sestrin2 in the rats after myocardial infarction (MI) following endoplasmic reticulum (ER) stress activated.

  METHODS  MI group rats were induced by ligation of left anterior descending coronary artery (LAD), sham group rats were induced by the same procedure except LAD ligation. ER stress activated model in cardiomyocytes by treated with tunicamycin (Tunicamycin group), cardioyocytes by treated with PBS were Control group. Apoptotic cardiomyocytes were detected by terminal transferase UTP nick end labelling (TUNEL) assays and flow cytometric analysis, respectively. Glucose regulagted protein 78 (GRP78), CCAAT-enhancer binding protein homologous protein (CHOP) and sestrin2 protein expression were reavealed by western blot analyses.

  RESULTS  In MI rats with ER stress activated conferred increased levels of GRP78 (P < 0.01), CHOP (P < 0.01) sestrin2 (P < 0.01) protein expression.Cardiomyocytes apoptosis also showed increased (P < 0.01) after MI.In cardiomyocytes treated with tunicamycin, GRP78 (P < 0.01), CHOP (P < 0.05), sestrin2 (P < 0.01) protein expression upregulated significantly. Meanwhile, apoptotic rates was also increased (P < 0.01). Moreover, inhibition of sestrin2 in cardiomyocytes treated with tunicamycin, CHOP protein (P < 0.05) expression showed upregulated and apoptotic rates of cardiomyocytes was also increased (P < 0.05) compared with cardiomyocytes treated with tunicamycin alone.

  CONCLUSION  Endogenous sestrin2 is involved in inhibiting endoplasmic reticulum stress mediated apoptosis after myocardial infarction.