• Media type: E-Article
  • Title: Junctional Adhesion Molecule A Expressed on Human CD34 + Cells Promotes Adhesion on Vascular Wall and Differentiation Into Endothelial Progenitor Cells
  • Contributor: Stellos, Konstantinos; Langer, Harald; Gnerlich, Stephan; Panagiota, Victoria; Paul, Angela; Schönberger, Tanja; Ninci, Elena; Menzel, Dagmar; Mueller, Iris; Bigalke, Boris; Geisler, Tobias; Bültmann, Andreas; Lindemann, Stephan; Gawaz, Meinrad
  • Published: Ovid Technologies (Wolters Kluwer Health), 2010
  • Published in: Arteriosclerosis, Thrombosis, and Vascular Biology, 30 (2010) 6, Seite 1127-1136
  • Language: English
  • DOI: 10.1161/atvbaha.110.204370
  • ISSN: 1524-4636; 1079-5642
  • Origination:
  • Footnote:
  • Description: Objective— To investigate the role of junctional adhesion molecule A (JAM-A) on adhesion and differentiation of human CD34 + cells into endothelial progenitor cells. Methods and Results— Tissue healing and vascular regeneration is a multistep process requiring firm adhesion of circulating progenitor cells to the vascular wall and their further differentiation into endothelial cells. The role of JAM-A in platelet-mediated adhesion of progenitor cells was investigated by adhesion assays in vitro and with the help of intravital fluorescence microscopy in mice. Preincubation of human CD34 + progenitor cells with soluble JAM-A-Fc (sJAM-A-Fc) resulted in significantly decreased adhesion over immobilized platelets or inflammatory endothelium under high shear stress in vitro and after carotid ligation in vivo or ischemia/reperfusion injury in the microcirculation of mice. Human CD34 + cells express JAM-A, as defined by flow cytometry and Western blot analysis. JAM-A mediates differentiation of CD34 + cells to endothelial progenitor cells and facilitates CD34 + cell-induced reendothelialization in vitro. Pretreatment of human CD34 + cells with sJAM-A-Fc resulted in increased neointima formation 3 weeks after endothelial denudation in the carotid arteries of nonobese diabetic/severe combined immunodeficient mice. Conclusion— These results indicate that the expression of JAM-A on CD34 + cells mediates adhesion to the vascular wall after injury and differentiation into endothelial progenitor cells, a mechanism potentially involved in vascular regeneration. Human CD34 + cells express JAM-A, mediating their interaction with platelets and endothelial cells. Specifically, JAM-A expressed on human CD34 + progenitor cells regulates their adhesion over immobilized platelets or inflammatory endothelium under high shear stress in vitro and after carotid ligation in vivo or ischemia/reperfusion injury in the microcirculation of mice. Moreover, it mediates differentiation of CD34 + cells to endothelial progenitor cells and facilitates reendothelialization.