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Expression of nitric oxide related enzymes in coronary heart disease

X Chen1, F Niroomand, Z Liu

  • 1Department of Cardiology, University of Heidelberg, INF 410, 69120, Heidelberg, Germany.

Basic Research in Cardiology
|May 18, 2006
PubMed

Insights

In atherosclerosis, gene expression of enzymes involved in nitric oxide (NO) metabolism is altered. Key enzymes that increase harmful ADMA levels were upregulated, while those promoting NO synthesis were downregulated in heart tissue.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • Nitric oxide (NO) bioavailability is reduced in atherosclerosis.
  • Enzymes metabolizing NO and reactive oxygen species (ROS) are potential contributors to NO deficiency.
  • Altered gene expression patterns of these enzymes may underlie NO dysregulation in atherosclerosis.

Purpose of the Study:

  • To investigate the gene expression patterns of enzymes involved in NO and ROS metabolism in myocardial tissue from patients with and without coronary heart disease (CHD).
  • To determine if altered expression of these enzymes contributes to the pathophysiology of atherosclerosis.

Main Methods:

  • Myocardial tissue samples were obtained from patients with CHD and control subjects.
  • mRNA and protein levels of key enzymes (NOS1-3, arginase1, p22phox, GTPCH, SOD1-3, PRMT1-3, DDAH2) were analyzed using rt-PCR, real-time PCR, and Western blot.

Main Results:

  • All investigated enzymes were expressed in human myocardium.
  • NOS isoforms protein levels were decreased in CHD, with significant downregulation of NOS3 expression.
  • Expression of PRMT1 and PRMT3 was increased, while DDAH2 expression was reduced, potentially increasing ADMA levels.
  • Superoxide dismutase 3 (SOD3) was downregulated in CHD tissue.

Conclusions:

  • Atherosclerosis is associated with enhanced expression of genes that increase ADMA levels and reduced expression of genes that promote NO synthesis in myocardial tissue.
  • These findings provide insights into the molecular mechanisms of increased oxidative stress in atherosclerosis at the gene expression level.

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