Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy

FEBS Lett. 2010 Jun 3;584(11):2363-70. doi: 10.1016/j.febslet.2010.04.025. Epub 2010 Apr 14.

Abstract

Adipose tissue secretes a variety of bioactive factors, which can regulate cardiomyocyte hypertrophy via reactive oxygen species (ROS). In the present study we investigated whether apelin affects ROS-dependent cardiac hypertrophy. In cardiomyocytes apelin inhibited the hypertrophic response to 5-HT and oxidative stress induced by 5-HT- or H(2)O(2) in a dose-dependent manner. These effects were concomitant to the increase in mRNA expression and activity of catalase. Chronic treatment of mice with apelin attenuated pressure-overload-induced left ventricular hypertrophy. The prevention of hypertrophy by apelin was associated with increased myocardial catalase activity and decreased plasma lipid hydroperoxide, as an index of oxidative stress. These results show that apelin behaves as a catalase activator and prevents cardiac ROS-dependent hypertrophy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly / prevention & control*
  • Catalase / metabolism*
  • Hydrogen Peroxide / pharmacology*
  • Hypertrophy / metabolism
  • Hypertrophy, Left Ventricular / metabolism
  • Mice
  • Myocardium / metabolism
  • Myocytes, Cardiac / drug effects*
  • Oxidative Stress / drug effects*
  • Rats
  • Reactive Oxygen Species / metabolism
  • Serotonin / pharmacology

Substances

  • Reactive Oxygen Species
  • Serotonin
  • Hydrogen Peroxide
  • Catalase