Low-dose aspirin promotes endothelial progenitor cell migration and adhesion and prevents senescence

Cell Biol Int. 2008 Jul;32(7):761-8. doi: 10.1016/j.cellbi.2008.03.004. Epub 2008 Mar 29.


Circulating endothelial progenitor cells (EPCs) play a key role in restoring endothelial function and enhancing angiogenesis. However, the effects of low-dose aspirin on circulating EPCs are not well known. We investigated the effects of low-dose aspirin on EPC migration, adhesion, senescence, proliferation, apoptosis and endothelial nitric oxide synthase (eNOS) expression. EPC migration was detected by a modified Boyden chamber assay. EPC adhesion assay was performed by counting adherent cells on fibronectin-coated culture dishes. EPC senescence was assessed by both senescence-associated-beta-galactosidase staining and DAPI staining. EPC proliferation was analyzed by MTT assay. EPC apoptosis was evaluated by flow cytometric analysis. eNOS protein expression was measured by Western blotting analysis. Aspirin promoted EPC migratory and adhesive capacity at concentrations between 0.1 and 100micromol/L and prevented senescence at concentrations between 50 and 100micromol/L. Meanwhile, aspirin in a range of these concentrations did not affect EPC proliferation, apoptosis or eNOS expression. Our findings indicate that low-dose aspirin promotes migration and adhesion and delays the onset of senescence of EPCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Aspirin / pharmacology*
  • Cell Adhesion / drug effects
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Cellular Senescence / drug effects
  • Cyclooxygenase Inhibitors / pharmacology
  • Dose-Response Relationship, Drug
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Humans
  • Male
  • Nitric Oxide Synthase Type III / metabolism
  • Stem Cells / drug effects*
  • Stem Cells / metabolism


  • Cyclooxygenase Inhibitors
  • Nitric Oxide Synthase Type III
  • Aspirin