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

Jun Liu1, Dan-Dan Hao, Jin-Sheng Zhang

  • 1Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, PR China.

Biochemical and Biophysical Research Communications
|September 7, 2011
PubMed

Insights

Hydrogen sulphide (H(2)S) inhibits cardiomyocyte hypertrophy by increasing miR-133a and reducing reactive oxygen species (ROS). This finding reveals H(2)S as a potential therapeutic target for cardiovascular diseases.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Cell Biology

Background:

  • Hydrogen sulphide (H(2)S) is vital in cardiovascular health and disease.
  • The role of H(2)S in cardiomyocyte hypertrophy (CH) remains unexplored.

Purpose of the Study:

  • To investigate the effect of H(2)S on cardiomyocyte hypertrophy.
  • To elucidate the underlying molecular mechanisms of H(2)S in CH.

Main Methods:

  • Utilized NaHS as an H(2)S donor in a cardiomyocyte hypertrophy model.
  • Measured [(3)H]-leucine incorporation, cell surface area, and gene/microRNA expression (BNP, ANP, miR-21, miR-133a).
  • Assessed intracellular reactive oxygen species (ROS) levels and employed anti-miR133a inhibitor transfection.

Main Results:

  • NaHS pretreatment significantly reduced hypertrophy markers ([(3)H]-leucine incorporation, cell surface area, BNP mRNA).
  • H(2)S treatment decreased intracellular ROS and miR-21 expression.
  • NaHS increased ANP mRNA and miR-133a expression; anti-miR133a partially reversed these effects.

Conclusions:

  • Hydrogen sulphide (H(2)S) directly inhibits cardiomyocyte hypertrophy (CH).
  • The protective effects involve upregulating miR-133a and downregulating intracellular reactive oxygen species (ROS).
  • H(2)S presents a potential therapeutic strategy for CH and related cardiovascular conditions.

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