title: Endothelial progenitor cell-based neovascularization: implications for therapy.
abstract: Ischemic cardiovascular events are a major cause of death globally. Endothelial progenitor cell (EPC)-based approaches can result in improvement of vascular perfusion and might offer clinical benefit. However, although functional improvement is observed, the lack of long-term engraftment of EPCs into neovessels has raised controversy regarding their mechanism of action. We and others have hypothesized that after ischemic injury, EPCs induce neovascularization through the secretion of cytokines and growth factors, which act in a paracrine fashion and induce sprouting angiogenesis by the surrounding endothelium. In this concise review, we discuss the (patho)physiology of EPC-induced neovascularization and focus on the paracrine signals secreted by EPCs and the effects they elicit. In future therapies, clinical administration of these paracrine modulators using slow-release depots might induce neovascularization and might therefore hold promise for vascular regenerative medicine.
authors.affiliation: Stem Cell and Tissue Engineering Research Group, Department Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Hanzeplein 1 (EA11), NL-9713GZ Groningen, The Netherlands.
authors.forename: Guido
authors.initials: G
authors.lastname: Krenning
authors.forename: Marja J A
authors.initials: MJ
authors.lastname: van Luyn
authors.forename: Martin C
authors.initials: MC
authors.lastname: Harmsen
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000473:pathology / Q000628:therapy; D064987:Cell- and Tissue-Based Therapy / Q000379:methods*; D042783:Endothelial Cells / Q000166:cytology*; D006801:Humans; D017202:Myocardial Ischemia / Q000473:pathology / Q000628:therapy; D018919:Neovascularization, Physiologic / Q000502:physiology*; D019899:Paracrine Communication / Q000502:physiology; D013234:Stem Cells / Q000166:cytology*