title: Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a.
abstract: Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS.
authors: Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, PR China.
authors: Jun
authors: J
authors: Liu
authors: Dan-Dan
authors: DD
authors: Hao
authors: Jin-Sheng
authors: JS
authors: Zhang
authors: Yi-Chun
authors: YC
authors: Zhu
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology*; D002460:Cell Line; D006862:Hydrogen Sulfide / Q000378:metabolism*; D006984:Hypertrophy / Q000378:metabolism / Q000473:pathology; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D020097:Natriuretic Peptide, Brain / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: C549446:MIRN133 microRNA, rat; D035683:MicroRNAs; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D013440:Sulfides; D020097:Natriuretic Peptide, Brain; C025451:sodium bisulfide; D006862:Hydrogen Sulfide