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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Angiogenesis. 2014 Nov 25;18(2):137–150. doi: 10.1007/s10456-014-9451-4

Figure 8. Candesartan enhanced VEGFR2 activity and stimulated proangiogenic effect.

Figure 8

Representative images of Western blot of the pVEGFR2 (on the same membrane in different positions) and their statistical analysis for the protein expression in normoxia (A, B) and hypoxia (C, D) respectively normalized to the corresponding total-VEGFR2. Treatment with candesartan significantly enhanced the VEGF-R2 activity in normoxia and hypoxia but not with siRNA in both. (E, F) Quantitative charts of tube-like structures formed in the same treatment groups (Corresponding representative images are shown in supplementary fig.3). In normoxia, silencing of HO-1 does not modify tube-like structures compared to controls but candesartan treatment (1μg/ml) significantly increased (3-fold) the effect. (B). In response to hypoxia, a significant (2-fold) increase in tube-like structure compared to normoxia in controls. Silencing of HO-1 significantly (2-fold) reduces endothelial cell-tube formation and candesartan significantly (4.5-fold) abolished the effect compared to controls. Silencing of HO-1 in the presence of candesartan significantly (1.9-fold) reduced tube-like structures compared to controls indicating that candesartan angiogenic response is HO-1 dependent. Two-way ANOVA showed significant interaction between candesartan and gene silencing in VEGFR2 activation in EC, *p<0.05 vs other groups, n=3-6/group.