Figure 2
From: Slit2N and Robo4 regulate lymphangiogenesis through the VEGF-C/VEGFR-3 pathway
Slit2N attenuates VEGF-C-induced activation of VEGFR-3 in L-LECs. (A) Representative VEGFR-3 IP/Western blot analysis of phosphorylated VEGFR-3 in L-LECs after pretreatment with various concentrations of Slit2N, and incubation with VEGF-C [100 ng/ml]. Total VEGFR-3 used as loading control. (B) Quantitative analysis of VEGFR-3 IP/Western blot analysis of phosphorylated VEGFR-3 in L-LECs after pretreatment with various concentrations of Slit2N, and incubation with VEGF-C. Band intensities from Figure 2A were determined by densitometry. The ratio of p-VEGFR-3/total VEGFR-3 of L-LECs treated with VEGF-C alone (2nd lanes from the left) was set to “1” and the ratios of all other conditions were calculated vs. this experimental condition. Data represent the mean ± SD of 3 independent experiments (*p < 0.05; **p < 0.01). (C) Representative Western blot analysis of phosphorylated VEGFR-2 in L-LECs after pretreatment with various concentrations of Slit2N, and incubation with VEGF-C [100 ng/ml]. Total VEGFR-2 used as loading control. (D) Quantitative analysis of Western blot analysis of phosphorylated VEGFR-2 in L-LECs after pretreatment with various concentrations of Slit2N, and incubation with VEGF-C. Band intensities from Figure 2C were determined by densitometry. The ratio of p-VEGFR-2/total VEGFR-2 of L-LECs treated with VEGF-C alone (2nd lanes from the left) was set to “1” and the ratios of all other conditions were calculated vs. this experimental condition. Data represent the mean ± SD of 3 independent experiments.