Figure 3.

The effect of hepatic HIF1A ablation on retinovascular protection by DMOG at P17. A: Lectin staining shows typical OIR pathology manifested as capillary dropout/avascularity that was prevented by i.p. DMOG injection, demonstrated here as robust preservation of central capillaries. In contrast, the liver HIF-1α KO mouse developed typical OIR pathology, characterized by capillary dropout seen surrounding the optic nerve, that was not prevented by DMOG, as it was in WT. In vivo fluorescein angiograms highlight posterior avascularity in the OIR model WT mouse that was prevented by HIF PHDi by DMOG. Fluorescein angiography confirms results from lectin-stained retinas shown above and demonstrates that DMOG could not prevent capillary loss in the HIF-1α KO mouse as it did in the WT mouse. Computerized quantification (see Sears et al²⁴ for details) of avascular retinal area (B); retinal area with neovascular tufts (C); and vascular tortuosity (D) confirm the failure of DMOG to prevent OIR-associated vascular pathology. PBS, blue bars; DMOG, red bars. Data are expressed as means ± SEM (B-D). n = 20 eyes per group (B-D). ^∗∗P < 0.01, ^∗∗∗∗P < 0.0001, t-test.