The Journal of Experimental Medicine
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Published online 28 December 2004 doi:10.1084/jem.20041402
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 1, 63-72
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ARTICLE

 Role of ß2-integrins for homing and neovascularization capacity of endothelial progenitor cells

Emmanouil Chavakis1, Alexandra Aicher1, Christopher Heeschen1, Ken-ichiro Sasaki1, Ralf Kaiser1, Naual El Makhfi1, Carmen Urbich1, Thorsten Peters2, Karin Scharffetter-Kochanek2, Andreas M. Zeiher1, Triantafyllos Chavakis3, and Stefanie Dimmeler1

1 Molecular Cardiology, Dept. of Medicine III, University of Frankfurt, 60950 Frankfurt, Germany
2 Department of Dermatology and Allergology, University of Ulm, Ulm, 89069 Germany
3 Department of Internal Medicine I, University Heidelberg, 69117 Heidelberg, Germany

CORRESPONDENCE Stefanie Dimmeler: Dimmeler{at}em.uni-frankfurt.de

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 ß2-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 ß2-integrin–deficient mice are less capable of homing to sites of ischemia and of improving neovascularization. Preactivation of the ß2-integrins expressed on EPCs by activating antibodies augments the EPC-induced neovascularization in vivo. These results provide evidence for a novel function of ß2-integrins in postnatal vasculogenesis.

T. Chavakis' present address is Experimental Immunology Branch, National Cancer Institute/National Institutes of Health, Bethesda, MD 20892.

Abbreviations used: ß2–/–, ß2-integrin–deficient; EPC, endothelial progenitor cell; HUVEC, human umbilical vein endothelial cell; MNC, mononuclear cell; vWF, von Willebrand factor.


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