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Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery
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Effects of endothelin-1 on endothelial progenitor cell function.

Kyle J Diehl1, Brian R Weil, Christian M Westby

  • 1Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO, USA.

Clinical Chemistry and Laboratory Medicine
|June 19, 2012
PubMed
Summary

Endothelin-1 (ET-1) does not impact endothelial progenitor cell (EPC) function but increases EPC apoptosis via an NADPH-dependent pathway. This heightened EPC apoptosis may promote atherosclerosis.

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Published on: April 13, 2012

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Vascular Biology

Background:

  • Circulating endothelial progenitor cells (EPCs) are crucial for vascular repair.
  • Endothelin (ET)-1 is implicated in endothelial damage and the development of atherosclerosis.

Purpose of the Study:

  • To investigate the in vitro effects of ET-1 on EPC colony formation, migration, angiogenic growth factor release, and apoptosis.

Main Methods:

  • Human peripheral blood-derived EPCs were isolated.
  • Assays included EPC colony-forming capacity, migratory activity, angiogenic factor release, and apoptosis.
  • Cells were treated with ET-1 (100 pmol) with and without receptor blockade or NADPH inhibition.

Main Results:

  • ET-1 did not significantly alter EPC colony formation, migration, or release of vascular endothelial growth factor and granulocyte-colony stimulating factor.
  • ET-1 significantly increased EPC apoptosis by 20%.
  • The proapoptotic effect of ET-1 was reversed by ET receptor blockade and apocynin (NADPH inhibitor).

Conclusions:

  • ET-1 does not impair EPC colony formation, migration, or angiogenic potential.
  • ET-1 enhances EPC apoptosis through an NADPH-dependent mechanism.
  • Increased EPC apoptosis induced by ET-1 may contribute to its proatherogenic effects.