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Arginase blockade lessens endothelial dysfunction after thrombosis.

Chandani Lewis1, Weifei Zhu, Mircea L Pavkov

  • 1Department of Cell Biology, the Lerner Research Institute, Cleveland, Ohio; Department of Vascular Surgery, Cleveland Clinic, Cleveland, Ohio, USA.

Journal of Vascular Surgery
|May 20, 2008
PubMed
Summary
This summary is machine-generated.

Acute arterial thrombosis increases arginase activity, leading to endothelial dysfunction. Blocking arginase activity restores normal arterial function, suggesting a therapeutic target for thrombosis-related vascular issues.

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Area of Science:

  • Vascular Biology
  • Endothelial Function
  • Thrombosis Research

Background:

  • Acute arterial thrombosis impairs endothelial function by reducing nitric oxide (NO) bioavailability.
  • Increased arginase activity may deplete L-arginine, the substrate for NO synthesis, contributing to endothelial dysfunction.

Purpose of the Study:

  • To investigate the role of arginase in endothelial dysfunction induced by thrombus formation.
  • To assess the impact of arginase inhibition on vasomotor responses in arteries affected by thrombosis.

Main Methods:

  • Rat aortic endothelial cells were exposed to thrombin to analyze arginase I expression.
  • In vivo, adult rats developed infrarenal aortic thrombosis.
  • Vascular reactivity of isolated aortic ring segments was measured using a force transducer, assessing endothelial-dependent relaxation (EDR) before and after arginase blockade.

Main Results:

  • Thrombin exposure significantly increased arginase I mRNA and protein levels in endothelial cells.
  • Arterial thrombosis led to diminished EDR in aortic ring segments, with a 3.8-fold increase in arginase I protein.
  • Arginase inhibition with difluoromethylornithine or [S]-[2-boronoethyl]-L-Cysteine-HCl (BEC) restored EDR to normal levels, while endothelial-independent relaxation remained unaffected.

Conclusions:

  • Endothelial cells exhibit increased arginase I expression upon thrombin stimulation.
  • Arterial thrombosis induces endothelial dysfunction, independent of smooth muscle responsiveness.
  • Arginase blockade effectively normalizes arterial vasomotor function in the presence of thrombosis.