Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a

Biochem Biophys Res Commun. 2011 Sep 23;413(2):342-7. doi: 10.1016/j.bbrc.2011.08.101. Epub 2011 Aug 27.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly / metabolism*
  • Cardiomegaly / pathology*
  • Cell Line
  • Hydrogen Sulfide / metabolism*
  • Hypertrophy / metabolism
  • Hypertrophy / pathology
  • MicroRNAs / biosynthesis*
  • MicroRNAs / genetics
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology*
  • Natriuretic Peptide, Brain / biosynthesis
  • Natriuretic Peptide, Brain / genetics
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Rats
  • Reactive Oxygen Species / metabolism
  • Sulfides / pharmacology
  • Up-Regulation


  • MIRN133 microRNA, rat
  • MicroRNAs
  • RNA, Messenger
  • Reactive Oxygen Species
  • Sulfides
  • Natriuretic Peptide, Brain
  • sodium bisulfide
  • Hydrogen Sulfide