Sestrin 2 attenuates neonatal rat cardiomyocyte hypertrophy induced by phenylephrine via inhibiting ERK1/2
Sestrin 2 attenuates neonatal rat cardiomyocyte hypertrophy induced by phenylephrine via inhibiting ERK1/2
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DOI：
10.1007/s11010-017-3020-2
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Liu C
中科院分区：
文献类型：
--
作者：
Dong B;Xue R;Sun Y;Dong Y;Liu C
Cardiac hypertrophy is an adaptive response triggered by many physiological and pathological conditions and will lead to heart failure eventually. Sestrin 2, which is a stress-responsive protein, was reported to protect heart from ischemia reperfusion injury. However, the role of Sestrin 2 in cardiac hypertrophy remains unknown. In our present study, we aimed to explore the effects of Sestrin 2 on cardiomyocyte hypertrophy. We found that knockdown of Sestrin 2 protein aggravated cardiomyocyte hypertrophy induced by phenylephrine (PE), featured by increased hypertrophic marker ANP and cell surface area. During this process, ERK1/2 cascade was further activated, while p38, JNK1/2, and mTOR signaling pathways were not affected by downregulation of Sestrin 2. Moreover, overexpression of Sestrin 2 protein protected cardiomyocytes from PE-induced hypertrophy and ERK1/2 cascade was suppressed correspondingly. Importantly, pharmacological inhibition of ERK1/2 eliminated the exacerbated hypertrophic phenotype due to Sestrin 2 protein knockdown. In conclusion, we discovered that Sestrin 2 protected against cardiomyocyte hypertrophy induced by PE via inhibiting ERK1/2 signaling.
