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. 2015 Apr 14;6(15):13790–13802. doi: 10.18632/oncotarget.3831

Figure 2. ARPCA inhibits the angiogenic activity of FGF8b.

Figure 2

A. HUVECs were stimulated with 30 ng/ml FGF8b in the presence of 60 μM ARPCA or ARPVA and immunostained with anti-FGFR1 (green) or anti-pFGFR1 (red) antibodies. Scale bar: 30 μm. Intensity of pFGFR1/FGFR1 signal was quantified and normalized to DAPI area (DAPI is in blue). The boxes extend from the 25th to the 75th percentiles, the lines indicate the median values, and the whiskers indicate the range of values. NS= not stimulated. B. Viable cell counting of HUVECs treated for 48 h with ARPCA or ARPVA in the presence of 30 ng/ml FGF8b. C. HUVEC spheroids were embedded in fibrin gel and treated with 30 ng/ml FGF8b or VEGF-A in the absence or presence of 60 μM ARPCA or ARPVA. After 24 h of stimulation the number of HUVEC sprouts were counted. D. Alginate pellets containing 4.5 pmoles of FGF8b or VEGF-A in the absence or presence of the indicated doses of ARPCA or ARPVA were placed on the top of the chick embryo CAM at day 11 of incubation. At day 14 newly formed blood vessels converging towards the implants were counted (8 embryos/group). Representative images of CAMs treated with FGF8b in the absence or presence of 140 pmoles of ARPCA or ARPVA are shown on the right. Data are the mean ± SEM. **P < 0.01 vs NS; §P < 0.05 vs FGF8b and +ARPVA; *P < 0.05; #P < 0.001.