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PARP1 interacts with HMGB1 and promotes its nuclear export in pathological myocardial hypertrophy

	author = {Qian Li and Zhuo-ming Li and Shu-ya Sun and Lu-ping Wang and Pan-xia Wang and Zhen Guo and Han-wei Yang and Jian-tao Ye and Jing Lu and Pei-qing Liu},
	title = {PARP1  interacts  with HMGB1  and promotes  its nuclear  export in pathological  myocardial  hypertrophy},
	journal = {Acta Pharmacologica Sinica},
	volume = {40},
	number = {5},
	year = {2019},
	keywords = {},
	abstract = {High-mobility group box 1 (HMGB1) exhibits various functions  according to its subcellular location, which is finely conditioned by diverse post-translational  modifications,  such as acetylation. The nuclear HMGB1 may prevent from cardiac hypertrophy, whereas its exogenous protein is proven to induce hypertrophic response. This present study sought to investigate the regulatory relationships between poly(ADP-ribose) polymerase 1 (PARP1) and HMGB1 in the process of pathological myocardial hypertrophy. Primary-cultured neonatal rat cardiomyocytes (NRCMs) were respectively incubated with three cardiac hypertrophic stimulants, including angiotensin  II (Ang II), phenylephrine  (PE), and isoproterenol (ISO), and cell surface area and the mRNA expression of hypertrophic biomarkers were measured. the catalytic activity of PARP1 was remarkably enhanced, meanwhile  HMGB1 excluded from the nucleus.  PARP1 overexpression by infecting with adenovirus PARP1 (Ad-PARP1) promoted the nuclear export of HMGB1, facilitated its secretion outside the cell, aggravated cardiomyocyte hypertrophy, which could be alleviated by HMGB1 overexpression.  PE treatment led to the similar results, while that effect was widely depressed by PARP1 silencing  or its specific inhibitor AG14361. Moreover,  SD rats were intraperitoneally injected with 3-aminobenzamide (3AB, 20 mg/kg every day, a well- established  PARP1 inhibitor) 7 days after abdominal aortic constriction  (AAC) surgery for 6 weeks, echocardiography  and morphometry of the hearts were measured. Pre-treatment of 3AB relieved AAC-caused the translocation of nuclear HMGB1 protein, cardiac hypertrophy, and heart dysfunction. Our research offers a novel evidence that PARP1 combines  with HMGB1 and accelerates its translocation from nucleus to cytoplasm, and the course finally causes cardiac hypertrophy.},
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