Platelets modulate atherogenesis and progression of atherosclerotic plaques via interaction with progenitor and dendritic cells

Platelets not only play a role in the late complications of atherosclerosis, but are also essential in its initiation, interacting with endothelial cells and leukocytes. Platelet adhesion to injured or atherosclerotic vessels is critical for the initiation of atherosclerotic lesion formation in vivo. Increasing evidence has recently highlighted the role of progenitor cells in inflammation, atherogenesis, and atheroprogression. Recruitment of progenitor and dendritic cells to sites of vascular injury is poorly understood so far. Both human progenitor and dendritic cells significantly adhere to platelets, indicating that platelets adherent to collagen or to endothelial cells can serve as a bridging mechanism directing circulating progenitor and dendritic cells to sites of impaired vasculature. Moreover, platelets regulate differentiation of progenitor cells to endothelial cells or macrophages and foam cells and modulate essential functions of dendritic cells, including their activation, differentiation and apoptosis in vitro. This review describes recent findings on platelet interaction with progenitor cells or dendritic cells and discusses potential consequences of this interaction in atherosclerosis.