Fig. 2

CIH inhibits the revascularization of ischemic retina, promotes pathological intravitreal neovascularization, and induces a transient growth retardation. (A) Schematic of the time course of OIR, normoxia, and CIH conditions. (B) Representative retinal flatmounts labeled with isolectin to visualize vessels. Avascular areas are indicated with a dashed orange line. PN18 insets show examples of neovascularization. PN30 insets highlight abnormal vasculature in some revascularized areas in OIR-CIH retinas. Quantification of (C) avascular and (D) neovascular regions in retinal flatmounts (n = 14–30 retinas per timepoint per group; two-way ANOVA followed by Šídák’s multiple comparisons test C * p = 0.0125 PN18 OIR-Norm versus OIR-CIH, $ p = 0.0014 PN21 OIR-Norm versus OIR-CIH, % p < 0.0001, D * p = 0.0028 PN24 OIR-Norm versus OIR-CIH, $ p = 0.0089 PN27 OIR-Norm versus OIR-CIH). In C the average percentage of avascular area at the end of OIR (PN13) is indicated with a blue dashed line. (E) Body weight in grams of pups from PN14-PN30 (n = 6–12 animals per group; two-way ANOVA followed by Šídák’s multiple comparisons test * p < 0.0001 PN16 OIR-Norm versus OIR-CIH, * p = 0.0001 PN18 OIR-Norm versus OIR-CIH, * p < 0.0001 PN21 OIR-Norm vs. OIR-CIH, * p < 0.0001 PN24 OIR-Norm versus OIR-CIH). Scales bars = 1000 μm; all values displayed as mean ± SEM, individual points indicate values per retina (C-D) or per animal (E)