Role of beta2-integrins for homing and neovascularization capacity of endothelial progenitor cells

J Exp Med. 2005 Jan 3;201(1):63-72. doi: 10.1084/jem.20041402. Epub 2004 Dec 28.

Abstract

The mechanisms of homing of endothelial progenitor cells (EPCs) to sites of ischemia are unclear. Here, we demonstrate that ex vivo-expanded EPCs as well as murine hematopoietic Sca-1+/Lin- progenitor cells express beta2-integrins, which mediate the adhesion of EPCs to endothelial cell monolayers and their chemokine-induced transendothelial migration in vitro. In a murine model of hind limb ischemia, Sca-1+/Lin- hematopoietic progenitor cells from beta2-integrin-deficient mice are less capable of homing to sites of ischemia and of improving neovascularization. Preactivation of the beta2-integrins expressed on EPCs by activating antibodies augments the EPC-induced neovascularization in vivo. These results provide evidence for a novel function of beta2-integrins in postnatal vasculogenesis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD18 Antigens / metabolism*
  • CD18 Antigens / physiology
  • Cell Adhesion / physiology
  • Cell Movement / physiology*
  • Endothelial Cells / metabolism
  • Endothelial Cells / physiology*
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / physiology
  • Flow Cytometry
  • Hindlimb / blood supply
  • Hindlimb / pathology
  • Humans
  • Ischemia / physiopathology*
  • Leukocytes, Mononuclear
  • Mice
  • Neovascularization, Physiologic / physiology*
  • Oligonucleotide Array Sequence Analysis
  • Stem Cells / metabolism
  • Stem Cells / physiology*

Substances

  • CD18 Antigens