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Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells

Ayşe Erol1, Mehtap G Cinar, Cenk Can

  • 1Department of Pharmacology and Clinical Pharmacology, School of Medicine, Ege University, Izmir, Turkey. ayse.erol@ege.edu.tr

Endothelium : Journal of Endothelial Cell Research
|June 21, 2007
PubMed

Insights

High homocysteine levels increase nitric oxide (NO) release from stimulated coronary microvascular endothelial cells (CMECs), likely involving reactive oxygen species. This suggests endothelial cells may produce NO to mitigate homocysteine-induced damage.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Function
  • Biochemistry

Background:

  • Hyperhomocysteinemia is a known risk factor for coronary artery disease.
  • The precise mechanisms linking homocysteine to cardiovascular damage remain unclear.
  • Understanding homocysteine's impact on endothelial function is crucial.

Purpose of the Study:

  • To investigate the effect of homocysteine on nitric oxide (NO) production in coronary microvascular endothelial cells (CMECs).
  • To explore the mechanisms underlying homocysteine's influence on NO release.
  • To determine if homocysteine affects basal or stimulated NO production.

Main Methods:

  • Isolated and cultured rat CMECs using the Langendorff system.
  • Assessed NO production by measuring nitrite accumulation via Griess reaction.
  • Evaluated the impact of varying homocysteine concentrations (0.01–1 mM) on basal and stimulated NO release.
  • Investigated the roles of L-NAME, superoxide dismutase, and catalase in modulating homocysteine's effects.

Main Results:

  • Homocysteine did not alter basal nitrite levels in CMECs.
  • A significant increase in stimulated nitrite accumulation was observed at 1 mM homocysteine.
  • This homocysteine-induced NO release was attenuated by L-NAME, superoxide dismutase, and catalase.
  • Results suggest increased reactive oxygen species production alongside NO release.

Conclusions:

  • Homocysteine stimulates NO release from CMECs, particularly under inflammatory or ionophore stimulation.
  • The effect is linked to increased reactive oxygen species production.
  • Endothelial cells may generate NO as a protective response to homocysteine-induced stress.

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