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Senescence marker protein 30 inhibits angiotensin II-induced cardiac hypertrophy and diastolic dysfunction.

Abstract：

BACKGROUND AND OBJECTIVE:Senescence marker protein 30 (SMP30) is assumed to behave as an anti-aging factor. Recently, we have demonstrated that deficiency of SMP30 exacerbates angiotensin II-induced cardiac hypertrophy, dysfunction and remodeling, suggesting that SMP30 may have a protective role in the heart. Thus, this study aimed to test the hypothesis that up-regulation of SMP30 inhibits cardiac adverse remodeling in response to angiotensin II. METHODS:We generated transgenic mice with cardiac-specific overexpression of SMP30 gene using α-myosin heavy chain promoter. Transgenic mice and wild-type littermate mice were subjected to continuous angiotensin II infusion (800 ng/kg/min). RESULTS:After 14 days, heart weight and left ventricular weight were lower in transgenic mice than in wild-type mice, although blood pressure was similarly elevated during angiotensin II infusion. Cardiac hypertrophy and diastolic dysfunction in response to angiotensin II were prevented in transgenic mice compared with wild-type mice. The degree of cardiac fibrosis by angiotensin II was lower in transgenic mice than in wild-type mice. Angiotensin II-induced generation of superoxide and subsequent cellular senescence were attenuated in transgenic mouse hearts compared with wild-type mice. CONCLUSIONS:Cardiac-specific overexpression of SMP30 inhibited angiotensin II-induced cardiac adverse remodeling. SMP30 has a cardio-protective role with anti-oxidative and anti-aging effects and could be a novel therapeutic target to prevent cardiac hypertrophy and remodeling due to hypertension.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Misaka T,Suzuki S,Miyata M,Kobayashi A,Ishigami A,Shishido T,Saitoh S,Kubota I,Takeishi Y

doi

10.1016/j.bbrc.2013.08.002

subject

Has Abstract

pub_date

2013-09-13 00:00:00

pages

142-7

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(13)01318-1

journal_volume

439

pub_type

杂志文章

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