SIRT3 inhibits cardiac hypertrophy by regulating PARP-1 activity.

Aging
Xiaojun FengSheng Liu

Abstract

Sirtuin 3 (SIRT3) is a type III histone deacetylase that inhibits cardiac hypertrophy. It is mainly localized in the mitochondria and is thus implicated in mitochondrial metabolism. Recent studies have shown that SIRT3 can also accumulate in the nuclear under stressed conditions, and participated in histone deacetylation of target proteins. Poly [ADP-ribose] polymerase 1 (PARP-1) functions as an important PARP isoform that was involved in cardiac hypertrophy. Our experiments showed that SIRT3 accumulated in the nuclear of cardiomyocytes treated with isoproterenol or SIRT3 overexpression. Moreover, overexpression of SIRT3 by adenovirus inhibited the expression of cardiac hypertrophic genes-ANF and BNP, as well as abrogating PARP-1 activation induced by isoproterenol or phenylephrine. In addition, co-immunoprecipitation experiments revealed that SIRT3 could interact with PARP-1, and overexpression of SIRT3 could decrease the acetylation level of PARP-1. Our results indicate that SIRT3 exerts protective effects against cardiac hypertrophy by reducing the level of acetylation and activity of PARP-1, thus providing novel mechanistic insights into SIRT3-mediated cardiprotective actions.

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Citations

Jan 29, 2021·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Jie ChenJunwei Liu
Jun 20, 2020·Biochimica Et Biophysica Acta. General Subjects·Ashlesha KadamRasheedunnisa Begum

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Methods Mentioned

BETA
acetylation
transfection
co-immunoprecipitation
ribosylation
PCR
co-IP

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