Figure 2
Figure 2. uPA-dependent cell survival is PI3 kinase independent. (A) HUMECs recovered after 24 hours from cultures seeded subconfluently on vitronectin (5000) in the absence or presence of the PI3 kinase inhibitor LY294002 (10 μM) and treated with either uPA (100 nM) or VEGF165 (1.25 nM). The effect of uPA was independent of the presence of the PI3 kinase inhibitor (*P < .01 vs control; n = 3). (B) Percentage of apoptotic HUMECs seeded on vitronectin for 24 hours in the absence or presence of the PI3 kinase inhibitor LY294002 (10 μM) and treated with either uPA (100 nM) or VEGF165 (1.25 nM). The effect of uPA in reducing the percentage of apoptotic cells was independent of the presence of the PI3 kinase inhibitor (*P < .01; n = 3). (C) Representative Western blot for pSer473 Akt in endothelial cells treated with uPA (100 nM) or VEGF165 (1.25 nM) and in the absence or presence of the specific PI3-kinase inhibitor LY294002 (10 μM). uPA did not induce Ser473 phosphorylation of Akt after 10 minutes (n = 3).

uPA-dependent cell survival is PI3 kinase independent. (A) HUMECs recovered after 24 hours from cultures seeded subconfluently on vitronectin (5000) in the absence or presence of the PI3 kinase inhibitor LY294002 (10 μM) and treated with either uPA (100 nM) or VEGF165 (1.25 nM). The effect of uPA was independent of the presence of the PI3 kinase inhibitor (*P < .01 vs control; n = 3). (B) Percentage of apoptotic HUMECs seeded on vitronectin for 24 hours in the absence or presence of the PI3 kinase inhibitor LY294002 (10 μM) and treated with either uPA (100 nM) or VEGF165 (1.25 nM). The effect of uPA in reducing the percentage of apoptotic cells was independent of the presence of the PI3 kinase inhibitor (*P < .01; n = 3). (C) Representative Western blot for pSer473 Akt in endothelial cells treated with uPA (100 nM) or VEGF165 (1.25 nM) and in the absence or presence of the specific PI3-kinase inhibitor LY294002 (10 μM). uPA did not induce Ser473 phosphorylation of Akt after 10 minutes (n = 3).

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