Close Encounters of the Third Kind

Abstract

Following vascular injury, endothelial cells become activated in the attempt to repave the damaged luminal surface. In addition, a physical interaction is established not only among the denuded subendothelial matrix, activated platelets, and circulating inflammatory cells but also with the progenitor cells (PCs).1 Endothelial survival, proliferation, and migration, necessary for re-coverage of exposed lamina, are aided by CD34+ PCs that express the vascular endothelial growth factor (VEGF) receptor-2/kinase-insert domain receptor (KDR). However, whether these cells enter the peripheral circulation as a predefined population or acquire their final antigenic phenotype on homing to the peripheral vasculature remains a matter of debate. See accompanying article on page 408 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , de Boer et al propose that human CD34+/KDR+ cells are generated from circulating CD34+ cells after immobilization on activated platelets.2 By using an ex vivo flow model, the authors show that activated platelets favor the homing of CD34+ cells to sites of vascular injury and that, on cell immobilization, KDR is rapidly translocated from an endosomal compartment to the cell surface. Presumably, PCs shed afterward to “carry the message” into the circulation. It is noteworthy that de Boer et al also report an increased coexpression of KDR on CD34+ cells in type-2 diabetes, which was reduced by aspirin treatment. The authors conclude that their data might have implications for the identification of patients with subclinical vascular injury, on the basis of the hypothesis that activated/injured endothelium provides more opportunity …