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Hypoxia-induced activation of the HIF transcription factor and angiogenesis are important events in the pathophysiology of wound healing, atherosclerosis and solid tumor growth. In the case of wound healing, this activation promotes angiogenesis at the wound bed to facilitate repair. Similarly, HIF activation during ischemia promotes the formation of new blood vessels to meet the tissue demands of oxygenation in response to this ischemic insult. On the other hand, HIF activation in neoplasia is associated with the induction of pro-angiogenic factors, such as VEGF, that stimulates the growth of new blood vessels to support the growth of the tumor. While it has been shown that transcription factor-mediated induction of the angiogenic switch promotes wound healing and tumor growth, the exact mechanism by which this occurs is largely unknown. Such a mechanism would be particularly useful to enable modulation of angiogenic factor induction by therapeutic means. One such therapeutic approach to promoting angiogenesis is to employ pro-angiogenic compounds to stimulate endothelial cell growth. For example, the angiogenic factors basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) promote wound healing (10, 23). Other pro-angiogenic factors including insulin-like growth factor (IGF-1), transforming growth factor (TGF-β), TGF-α and TGF-β activate endothelial cells to proliferate and migrate, enhancing the formation of new blood vessels (8, 30-34). Many of the pro-angiogenic factors involved in wound healing or tumor growth, such as VEGF, bFGF and IGF-1, act as paracrine regulators that are highly active in their target tissue and are rapidly metabolized upon their release from the site of synthesis. Thus, in the case of wound healing, these factors are only active in the immediate vicinity of the wound, and are present at very low concentrations. In contrast, pro-angiogenic factors produced by tumors are active at much higher levels, and have the capacity to diffuse away from the site of their production to act at distal sites. Accordingly, it is desirable to provide a mechanism by which to increase the local concentration of pro-angiogenic compounds in the vicinity of the target tissue, to more efficiently promote wound healing or tumor growth. In the case of solid tumors, the release of pro-angiogenic factors from the tumor is likely



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