Granulocyte colony-stimulating factor-mobilized circulating c-Kit+/Flk-1+ progenitor cells regenerate endothelium and inhibit neointimal hyperplasia after vascular injury

Arterioscler Thromb Vasc Biol. 2006 Apr;26(4):751-7. doi: 10.1161/01.ATV.0000205607.98538.9a. Epub 2006 Jan 26.

Abstract

Background: Granulocyte colony-stimulating factor (G-CSF) treatment was shown to inhibit neointimal formation of balloon-injured vessels, whereas neither the identification of progenitor cells involved in G-CSF-mediated endothelial regeneration with a bone marrow (BM) transplant experiment nor the functional properties of regenerated endothelium have been studied.

Methods and results: Recombinant human G-CSF (100 microg/kg per day) was injected daily for 14 days starting 3 days before balloon injury in the rat carotid artery. Neointimal formation of denuded vessels on day 14 was markedly attenuated by G-CSF (39% versus the control; P<0.05). Endothelial cell-specific immunostaining revealed an enhancement of re-endothelialization (1.8-fold increase versus the control; P<0.05) and inhibition of extravasation of Evans Blue dye (47%; P=0.02). The regenerated endothelium exhibited acetylcholine-mediated vasodilatation in NO-dependent manner. G-CSF increased the circulating c-Kit+/Flk-1+ cells (9.1-fold; P<0.02), which showed endothelial properties in vitro (acetylated low-density lipoprotein uptake and lectin binding) and incorporated into the regenerated endothelium in vivo. A BM replacement experiment with green fluorescent protein (GFP)-overexpressing cells showed that BM-derived GFP+/CD31+ endothelial cells occupied 39% of the total luminal length in the G-CSF-mediated neo-endothelium (2% in the control).

Conclusions: The G-CSF-induced mobilization of BM-derived c-Kit+/Flk-1+ cells contributes to endothelial regeneration, and this cytokine therapy may be a feasible strategy for the promotion of re-endothelialization after angioplasty.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carotid Artery Injuries / drug therapy*
  • Carotid Artery Injuries / pathology
  • Carotid Artery Injuries / physiopathology
  • Carotid Artery, Common / metabolism
  • Carotid Artery, Common / pathology
  • Carotid Artery, Common / physiology
  • Cell Proliferation
  • Cells, Cultured
  • Endothelium, Vascular / pathology
  • Granulocyte Colony-Stimulating Factor / administration & dosage*
  • Humans
  • Hyperplasia / prevention & control
  • Injections, Subcutaneous
  • Mice
  • Nitric Oxide Synthase Type III / metabolism
  • Proto-Oncogene Proteins c-kit
  • Rats
  • Rats, Inbred Lew
  • Recombinant Proteins
  • Regeneration*
  • Stem Cells / drug effects
  • Stem Cells / pathology
  • Tunica Intima / metabolism
  • Tunica Intima / pathology
  • Tunica Intima / physiopathology*
  • Vasodilation

Substances

  • Recombinant Proteins
  • Granulocyte Colony-Stimulating Factor
  • Nitric Oxide Synthase Type III
  • Proto-Oncogene Proteins c-kit