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PARP-2 knockdown protects cardiomyocytes from hypertrophy via activation of SIRT1.

Authors: Geng, Biao  Cai, Yi  Gao, Si  Lu, Jing  Zhang, Lu  Zou, Jian  Liu, Min  Yu, Shanshan  Ye, Jiantao  Liu, Peiqing 
Citation: Geng B, etal., Biochem Biophys Res Commun. 2013 Jan 18;430(3):944-50. doi: 10.1016/j.bbrc.2012.11.132. Epub 2012 Dec 19.
Pubmed: (View Article at PubMed) PMID:23261455
DOI: Full-text: DOI:10.1016/j.bbrc.2012.11.132

Poly(ADP-ribosyl)ation catalyzed by the poly(ADP-ribose) polymerases (PARPs) is an immediate post-translational modification of proteins with a homopolymeric chain of repeating ADP-ribose units. It is involved in various cellular processes, such as cell survival and death, transcription, DNA repair and cell division. Inhibitors of PARPs have been documented to be useful in different pathological conditions. Recently, activation of PARP-1, the founding member of PARP family, has been revealed to participate in the development and progression of cardiac hypertrophy and heart failure. However, the roles of other PARPs in cardiovascular system remain to be clarified. PARP-2 shares 69% similarity with PARP-1 in catalytic domains, but their functions do not fully overlap. In this study, we show the first evidence that PARP-2 is involved in cardiac hypertrophy. The mRNA and protein levels of PARP-2 were significantly increased in AngII-stimulated rat cardiomyocytes as well as in hearts of rats submitted to pressure overload. PARP-2 knockdown protected cardiomyocytes from hypertrophy, which may be attributed to activation of SIRT1. These findings shed new light on the understanding of PARP-2-related cardiomyopathy, and suggest the potential application of PARP-2 inhibitors in cardiac hypertrophy.

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CRRD Object Information
CRRD ID: 13514044
Created: 2018-03-21
Species: All species
Last Modified: 2018-03-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.