PERK-mediated endoplasmic reticulum stress is involved in angiotensin II-induced myocardial hypertrophy

AIM: To investigate the role of protein kinase R-like endoplasmic reticulum kinase (PERK)-mediated endoplasmic reticulum stress (ERS) in angiotensin II (AngⅡ) -induced myocardial hypertrophy. METHODS: In the hypertrophy model of AngⅡ-induced cardiomyocytes isolated from neonatal Sprague-Dawley rats, the methods of morphological observation, [³H]-leucine incorporation and surface area measurement were employed to assess the cardiomyocyte hypertrophy. Real-time PCR, RT-PCR and Western blotting were used to detected the expression of glucose-regulated protein 78 (GRP78), calreticulin (CRT), PERK, eukaryotic initiation factor 2α (eIF2α) and C/EBP homologous protein (CHOP) at mRNA and protein levels. RESULTS: Compared with control group, Ang II-treated cardiomyocytes showed that the mRNA and protein expression of CRT increased by 146.4% and 125.3%, respectively (P<0.05). The mRNA and protein expression of GRP78 increased by 84.0% and 77.6%, respectively (P<0.05). The mRNA and protein expression of PERK increased by 165.4% and 132.1%, respectively (P<0.05).The mRNA and protein expression of eIF2α was increased by 110.9% and 46.5%, respectively (P<0.05). The mRNA and protein expression of CHOP also increased by 117.7% and 63.3%, respectively (P<0.05). CONCLUSION: PERK-mediated ERS response is involved in AngⅡ-induced cardiomyocyte hypertrophy.