Research for this thesis was conducted to study the mechanism by which satellite cells affect angiogenesis via hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF). We found that satellite cells exposed to hypoxia and cobalt chloride (CoCl2) had increased HIF-1 activity, greater VEGF gene expression, and higher levels of VEGF protein secreted into conditioned medium, when compared to satellite cells cultured in normoxia. The biological role of VEGF protein in satellite cell-mediated angiogenesis was observed when the growth of microvascular sprouts in satellite cell conditioned medium was inhibited by the addition of VEGF soluble receptors. This inhibition could be reversed when recombinant VEGF protein was added. Taken together, these data suggest that satellite cells mediate angiogenesis through the secretion of VEGF protein, and VEGF secretion can be increased upon exposure to a hypoxic environment.
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