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Heme oxygenase-1 inhibits pro-oxidant induced hypertrophy in HL-1 cardiomyocytes

Keith R Brunt1, Matthew R Tsuji, Joyce H Lai

  • 1Department of Physiology, Queen's University, 431 Botterell Hall, Kingston, Ontario K7L 3N6, Canada.

Experimental Biology and Medicine (Maywood, N.J.)
|February 27, 2009
PubMed

Insights

Heme oxygenase-1 (HO-1) protects against reactive oxygen species (ROS)-induced cardiac hypertrophy. Overexpressing HO-1 in cardiomyocytes inhibited hypertrophy via a nuclear factor kappa B (NF-kappaB) dependent pathway.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Reactive oxygen species (ROS) are key mediators in cardiac hypertrophy.
  • Heme oxygenase-1 (HO-1) possesses significant antioxidant properties.

Purpose of the Study:

  • To investigate the hypothesis that HO-1 inhibits ROS-induced cardiomyocyte hypertrophy.
  • To elucidate the molecular mechanisms underlying HO-1's protective effects.

Main Methods:

  • HL-1 cardiomyocytes were transduced to overexpress HO-1.
  • Cells were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
  • Hypertrophy was assessed using multiple quantitative methods, including 3H-leucine incorporation and flow cytometry.
  • Redox balance and NF-kappaB activation were analyzed.

Main Results:

  • HO-1 overexpression significantly attenuated H2O2-induced redox imbalance.
  • Pre-emptive HO-1 expression reduced hypertrophic indices in cardiomyocytes.
  • This study provides the first direct evidence of HO-1 inhibiting oxidant-induced cardiomyocyte hypertrophy through a NF-kappaB-dependent mechanism.

Conclusions:

  • HO-1 effectively inhibits pro-oxidant-induced cardiomyocyte hypertrophy.
  • HO-1 demonstrates therapeutic potential for conditions involving oxidative stress and cardiac hypertrophy.
Abstract

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