Figure 7.

uPAR is not essential for antiendothelial cell activity of HKa. A) Proliferation of endothelial cells pretreated with control or uPAR siRNA. Cell proliferation was determined by counting of cells and comparison to cells treated with growth factors in the absence of siRNA. B) Inhibition of proliferation of endothelial cells pretreated with control or uPAR siRNA by HKa (15 nM). C) HKa-induced caspase activation in endothelial cells pretreated with control or uPAR siRNA. D) Immunoblots of uPAR immunoprecipitate from control endothelial cells incubated in medium alone, or endothelial cells induced to undergo apoptosis by HKa, staurosporine, or TNF-α, using antibody to integrin αVβ3. Coimmunoprecipitation of uPAR and integrin αVβ3 was reduced in response to all 3 agonists. E) Inhibition of angiogenesis by HKa in wild-type and uPAR^−/− mice. Matrigel plugs assays were performed as described in Materials and Methods. Figure depicts hemoglobin content in individual Matrigel plugs 9 d after plug placement. Each data point represents mean ± sem of 10 Matrigel plugs (2 plugs each placed into 5 mice per group). HKa inhibited angiogenesis equally well in wild-type and uPAR^−/− mice.