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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: Exp Eye Res. 2019 Aug 23;187:107775. doi: 10.1016/j.exer.2019.107775

Fig. 3. FGF2, but not FGF8 or FGF9 stimulates pathogenic CNV after laser induction.

Fig. 3.

FGF2 stimulated CNV formation following laser injury in C57Bl/6J mice in a dose-dependent manner, reaching significance at doses of 10 ng and 100 ng compared to mice receiving vehicle control (n=13–16; 40599.3 ± 4508.1 μm2 vs 82273.4 ± 17833.4 μm2, *p<0.01 (10ng) or 93878.9 ± 12475.6 μm2, *p<0.01 (100ng); one-way ANOVA with Bonferroni’s multiple comparison test (A). Neutralizing antibody against FGF2 significantly suppressed CNV formation (n=7–9; 30369.2 ± 5010.7 μm2 vs. 74338.9 ± 15250.2 μm2, *p<0.05; two-tailed Student’s unpaired t-test (B). Furthermore, CNV formation was impaired in Fgf2−/− mice as compare to its littermates (n=6–7; 93264 ± 7690 μm2 vs. 26699 ± 5958 μm2, †p<0.0001; two-tailed Student’s unpaired t-test) (C) while deletion of Fgf8 (D) (n=8; n.s.= no significance by two-tailed Student’s unpaired t-test) or Fgf9 (E) (n=13–15; n.s.= no significance by two-tailed Student’s unpaired t-test) did not significantly modify CNV volumes compared to their respective littermate controls. Scale bar: 200 μm.