UNIVERSITY OF MIAMI
Restoring blood flow to the site of injured tissue is a prerequisite for mounting a successful repair response. It is now well established that the sources of endothelial cells which build newly-formed blood vessels come from both pre-existing vessels (angiogenesis) and bone marrow-derived EPC (vasculogenesis). In addition to direct cellular contribution to new vessels, EPC secrete growth factors and cytokines that enhance angiogenesis and other wound healing processes via paracrine effects. EPC are the key cellular effectors of both reparative and pathologic postnatal neovascularization and play a pivotal role in not only wound healing, but also limb ischemia 2-4, post-myocardial infarction 5-7, endothelialization of vascular grafts 8,9, atherosclerosis 10, retinal and lymphoid organ neovascularization 11,12, vascularization during neonatal growth 13, and tumor growth 14,15. Our overall goal is to identify of novel targets for the regulation of post-natal neovascularization mediated by EPC in order to improve on the unsolved problem of Diabetes-associated delayed wound healing.