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Overexpression of eNOS decrease tissue factor (TF) level in CD34+ cells exhibit increased antithrombogenic property

Feng Wang1, Gang Li2, Xin Guan1

  • 1Department of Cardiothoracic Surgery, Shanghai Ninth People' s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.

The Journal of Cardiovascular Surgery
|September 5, 2015
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Summary
This summary is machine-generated.

Overexpressing endothelial nitric oxide synthase (eNOS) in endothelial progenitor cells (EPCs) reduces tissue factor (TF) and enhances antithrombogenic properties for vascular grafts.

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Area of Science:

  • Biomedical Engineering
  • Vascular Biology
  • Cell Therapy

Background:

  • Endothelial progenitor cells (EPCs) exhibit reduced eNOS expression, potentially impairing their antithrombogenic capacity for vascular grafts.
  • Investigating eNOS overexpression in EPCs is crucial for improving graft performance.

Purpose of the Study:

  • To determine if eNOS overexpression in EPCs enhances antithrombogenic properties.
  • To assess the effect of eNOS overexpression on tissue factor (TF) levels in EPCs.

Main Methods:

  • Isolated CD34+ cells and differentiated them into EPCs using VEGF.
  • Overexpressed eNOS via plasmid transfection in CD34+ cells.
  • Analyzed TF expression, platelet adhesion in vitro, and graft thrombopoiesis/fibrin adhesion in vivo.

Main Results:

  • eNOS gene transfection reduced TF levels in CD34+ cells, abrogating TNFα-induced TF expression.
  • Overexpression of eNOS significantly inhibited platelet adhesion in vitro.
  • In vivo studies showed decreased thrombopoiesis and fibrin adhesion on vascular grafts seeded with eNOS-overexpressing EPCs.

Conclusions:

  • Overexpression of eNOS effectively decreases TF levels in EPCs.
  • Enhanced eNOS expression improves the antithrombogenic properties of small-caliber vascular grafts.