Reduced number and impaired function of circulating endothelial progenitor cells in patients with abdominal aortic

Shih-Hsien Sung1, Tao-Cheng Wu, Jia-Shiong Chen

  • 1Division of Cardiology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Cardiovascular Research Center, National Yang-Ming University School of Medicine, Taipei, Taiwan; Institute of Public Health, National Yang-Ming University School of Medicine, Taipei, Taiwan.

Insights

The number and function of circulating endothelial progenitor cells (EPCs) are reduced in patients with abdominal aortic aneurysms (AAAs). Impaired EPCs suggest a potential role in AAA development and progression.

Area of Science:

  • Vascular Biology
  • Regenerative Medicine
  • Cardiovascular Research

Background:

  • Circulating endothelial progenitor cells (EPCs) are crucial for vascular repair and are linked to coronary artery disease (CAD).
  • Abdominal aortic aneurysm (AAA) shares risk factors with CAD, but its relationship with EPCs is not well understood.

Purpose of the Study:

  • To investigate the correlation between circulating EPCs and the presence and severity of AAA.
  • To assess the functional capacity of EPCs in AAA patients.

Main Methods:

  • Prospective enrollment of 78 subjects with suspected AAA.
  • Evaluation of endothelial function using flow-mediated vasodilation (FMD).
  • Quantification of circulating EPCs and colony-forming units (CFUs) via flow cytometry.
  • Assessment of late outgrowth EPC function (proliferation, adhesion, migration, tube formation, senescence) in a subset of patients.

Main Results:

  • AAA patients exhibited significantly lower FMD compared to controls.
  • Reduced numbers of circulating EPCs (CD34+/KDR+, CD133+/KDR+) and CFUs were observed in AAA patients.
  • EPC numbers (CFUs and CD34+/KDR+) were inversely correlated with AAA diameter.
  • Impaired proliferation, adhesion, migration, tube formation, and increased senescence were noted in late outgrowth EPCs from AAA patients.

Conclusions:

  • Both the number and function of EPCs are significantly impaired in patients with AAA.
  • These findings suggest a potential role for EPC dysfunction in the pathogenesis of AAA.
Abstract

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