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Nitric oxide-induced cell death in the heart: the role of autophagy

Simon W Rabkin1

  • 1Department of Medicine, University of British Columbia, Vancouver, Canada. rabkin@interchange.ubc.ca

Autophagy
|April 18, 2007
PubMed

Insights

Nitric oxide (NO) does not appear to increase beclin 1 expression during heart ischemia/reperfusion injury. This suggests NO is unlikely to cause autophagy observed in heart failure patients.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Autophagy Research

Background:

  • Autophagy is evident in human heart failure and experimental myocardial ischemia/reperfusion.
  • The role of autophagy in these conditions is debated, with conflicting data on Beclin 1's effect on cardiomyocyte injury.
  • Increased beclin 1 expression is consistently noted in myocardial ischemia/reperfusion.

Purpose of the Study:

  • To investigate if nitric oxide (NO) and peroxynitrite affect autophagy gene expression in the heart.
  • To determine the relationship between NO signaling and beclin 1 expression in cardiac injury models.

Main Methods:

  • Neonatal mouse cardiomyocytes were treated with SIN-1 to generate NO and peroxynitrite.
  • Gene expression changes were analyzed using cDNA microarrays.
  • Evaluated short (2h) and long (20h) treatment durations to model different injury scenarios.

Main Results:

  • SIN-1 treatment significantly altered the expression of five caspases.
  • No significant changes were observed in the expression of autophagy-related genes: beclin 1, Atg5l, and Atg12l.
  • These findings were consistent across both short and long treatment periods.

Conclusions:

  • NO does not appear to be involved in the upregulation of beclin 1 during myocardial ischemia/reperfusion.
  • NO is unlikely to be the cause of the observed autophagy in heart failure patients.

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