Role of β2-integrins for homing and neovascularization capacity of endothelial progenitor cells

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 β2-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 β2-integrin–deficient mice are less capable of homing to sites of ischemia and of improving neovascularization. Preactivation of the β2-integrins expressed on EPCs by activating antibodies augments the EPC-induced neovascularization in vivo. These results provide evidence for a novel function of β2-integrins in postnatal vasculogenesis.

The SDF-1–CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis

“…SDF-1 induces integrin expression on EPCs [18] in addition to vascular cell adhesion molecule-1 on the endothelium [52]. Other crucial integrins mediating the incorporation of EPCs include β2 integrins, lymphocyte function-associated antigen-1 and intercellular adhesion molecule-1 [53][54][55]. In addition, Massberg et al have demonstrated that SDF-1 released from platelets supports the recruitment of EPCs and facilitates their adhesion to the injured vascular wall [34].…”

QTL analyses of lineage-negative mouse bone marrow cells labeled with Sca-1 and c-Kit

“…and Itgb2, an integrin involved in HSC homing to the periphery (Chavakis et al 2005), leads to the tempting hypothesis that genetic variation in a common HSC homing pathway may be important in determining stem cell numbers. This hypothesis must remain tentative however until confirmatory laboratory experiments have been carried out.…”

Thérapies cellulaires pro-angiogéniques dans le traitement des pathologies ischémiques

“…Les chimiokines et les plaquettes permettent aussi la capture des CPE au niveau des zones de lésions vasculaires [15,16]. Une fois qu'elles ont été recrutées, les CPE se fixent sur l'endothélium activé par l'ischémie, grâce à l'action des molécules d'adhésion présentes sur la surface vasculaire comme l'intégrine 2 et la sélectine de type L [17][18][19]. Une fois adhérentes à Figure 1.…”