Figure 2.

Consequences of the postnatal down-regulation and inhibition of the sEH on retinal angiogenesis. (A) sEH^iKO mice were treated with tamoxifen from P1 to P4 and sEH expression was determined by Western blotting. Similar observations were obtained in 5 additional experiments. Retinas from wild-type and sEH^−/− mice were used as positive (PC) and negative (NC) controls, respectively. (B) Isolectin B4 staining in retinal whole mounts from tamoxifen-treated sEH^fl/fl and sEH^iKO mice on P5. Bar, 500 µm. (C) Quantification of vascularization. n = 5 total animals per group, from 3 different experiments. (D) Expression of genes involved in Notch signaling was assessed in P5 retinas by RT-qPCR. Each sample was a pool of 3 retinas, and the analysis was performed on 4 independent samples per genotype. (E) Wild-type mice were treated with vehicle (Veh) or sEH inhibitor (sEH-I) for 4 d and Isolectin B4 staining was analyzed by confocal microscopy. Bar, 500 µm. (F) Quantification of vascularization based in data in E. n = 5–9 total animals per group from 4 different experiments. (G) 5-d-old wild-type mice were treated with vehicle or sEH inhibitor for 4 d, and Notch pathway gene expression was assessed by RT-qPCR. Each sample was a pool of 3 retinas, and the analysis was performed on 6 independent samples per genotype. Error bars represent SEM. *, P < 0.05; **, P < 0.01 versus sEH^fl/fl mice or vehicle.