Figure 5
Figure 5. VEGF-induced XIAP mRNA up-regulation is uPA dependent. (A) Dose-dependent effect of VEGF165 (6 hours) on XIAP mRNA expression in HUVECs. Data represent fold increase over control (*P < .01, ANOVA; n = 3). (B) XIAP mRNA up-regulation in HUVECs by VEGF165 (1.25 nM) in the absence or presence of the specific PI3 kinase inhibitor LY294002 (10 μM) or the specific IKK inhibitor BAY 11-7085 (5 μM). XIAP up-regulation by VEGF165 is dependent on LY294002 and BAY 11-7085 (P < .01; n = 4). (C) miap3 (the mouse homolog of XIAP) mRNA up-regulation by mVEGF164 (1.25 nM) in wild-type or uPA−/− mouse endothelial cells. Data are shown as ratio of miap3 mRNA in VEGF-treated uPA−/− cells over miap3 mRNA in VEGF-treated wild-type control cells. VEGF induced up-regulation of miap3 mRNA is only approximately one-fifth in uPA-deficient cells (P < .01; n = 3).

VEGF-induced XIAP mRNA up-regulation is uPA dependent. (A) Dose-dependent effect of VEGF165 (6 hours) on XIAP mRNA expression in HUVECs. Data represent fold increase over control (*P < .01, ANOVA; n = 3). (B) XIAP mRNA up-regulation in HUVECs by VEGF165 (1.25 nM) in the absence or presence of the specific PI3 kinase inhibitor LY294002 (10 μM) or the specific IKK inhibitor BAY 11-7085 (5 μM). XIAP up-regulation by VEGF165 is dependent on LY294002 and BAY 11-7085 (P < .01; n = 4). (C) miap3 (the mouse homolog of XIAP) mRNA up-regulation by mVEGF164 (1.25 nM) in wild-type or uPA−/− mouse endothelial cells. Data are shown as ratio of miap3 mRNA in VEGF-treated uPA−/− cells over miap3 mRNA in VEGF-treated wild-type control cells. VEGF induced up-regulation of miap3 mRNA is only approximately one-fifth in uPA-deficient cells (P < .01; n = 3).

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