Angiotensin-Converting Enzyme 3 ( ACE 3 ) Protects Against Pressure Overload-Induced Cardiac Hypertrophy

Content Provider	Semantic Scholar
Author	Yu, Chang-Jiang Tang, Liang-Liang Liang, Chen Chen, Xiao Lin Song, Shu-Ying Ding, Xiao-Qing Zhang, Kun-Yu Song, Bin-Lin Zhao, Dan Zhu, Xue-Yong Li, Hongliang Zhang, Zhi-Ren
Copyright Year	2016
Abstract	Methods and Results-—Neonatal rat cardiomyocytes (NRCMs) with gain and loss of function of ACE3 and mice with global knockout or cardiac-specific overexpression of ACE3 were used in this study. In cultured cardiomyocytes, ACE3 conferred protection against angiotensin II (Ang II)-induced hypertrophic growth. Cardiac hypertrophy in mice was induced by aortic banding (AB) and the extent of hypertrophy was analyzed through echocardiographic, pathological, and molecular analyses. Our data demonstrated that ACE3-deficient mice exhibited more pronounced cardiac hypertrophy and fibrosis and a strong decrease in cardiac contractile function, conversely, cardiac-specific ACE3-overexpressing mice displayed an attenuated hypertrophic phenotype, compared with control mice, respectively. Analyses of the underlying molecular mechanism revealed that ACE3mediated protection against cardiac hypertrophy by suppressing the activation of mitogen-activated protein kinase kinase (MEK)regulated extracellular signal-regulated protein kinase (ERK1/2) signaling, which was further evidenced by the observation that inhibition of the MEK-ERK1/2 signaling by U0126 rescued the exacerbated hypertrophic phenotype in ACE3-deficient mice.
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Alternate Webpage(s)	http://jaha.ahajournals.org/content/ahaoa/5/2/e002680.full.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article