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... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Biochemistry Springer Journals

Sestrin 2 attenuates neonatal rat cardiomyocyte hypertrophy induced by phenylephrine via inhibiting ERK1/2

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Medical Biochemistry; Oncology; Cardiology
ISSN
0300-8177
eISSN
1573-4919
D.O.I.
10.1007/s11010-017-3020-2
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

Molecular and Cellular BiochemistrySpringer Journals

Published: May 11, 2017

References

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