The wide range of estimates on the relative contribution of bone marrow-derived cells to neovasculature suggests that this contribution may vary depending on the conditions in a particular experiment or the biological/clinical situation. One prevailing theme in the literature is the absence or low level of bone marrow-derived cells incorporated into quiescent endothelium, while higher percentages of marrow-derived cells are reported in proliferating vascula-ture. Other than this broad generalization, factors that may influence the relative contributions of angiogenesis and vas-culogenesis to neovessel formation in different circumstances remains unclear. One variable that may play a role is the number of circulating endothelial progenitors.
In a broad sense, the number of circulating endothelial progenitors is increased by vascular injury. More specifically, the levels of several cytokines have been found to influence the numbers of circulating EPCs. Not surprisingly, VEGF was one of the first substances identified that increases EPC number. Increased plasma levels of VEGF in adult mice and humans has been shown to increase EPCs. Other chemokines such as platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and interleukin-8 (IL-8) have also been shown to promote the migration of endothelial cells to sites of injury. G-CSF, GM-CSF, and erythropoietin, cytokines already in use clinically to promote mobilization of hematopoietic cells, can also increase EPCs. EPC mobilization can also be increased by HMG-CoA reductase inhibitors (statins). Further dissection of the mobilization of circulating EPCs by Heissig and colleagues shows that mobilization of both hematopoietic and endothelial precursors is dependent on MMP-9-mediated release of soluble kit ligand (sKitL) in the bone marrow.
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