Figure 1. VE-PTP is upregulated in hypoxic endothelial cells and plays an important role in ocular NV.
(A) After incubation in 5% oxygen for 0, 4, or 16 hours, hypoxic HUVECs showed an increase in VE-PTP. (B) GSA lectin–stained retinal NV in P17 mice with ischemic retinopathy stained for VE-PTP, with faint staining of preexistent retinal vessels (arrowheads). Scale bar: 100 μm. (C) Elimination of primary antibody eliminated staining. Scale bar: 100 μm. (D) Nonischemic retinas at P17 showed normal GSA-stained vessels, no NV, and no VE-PTP staining. Scale bar: 100 μm. (E) At P12, mice with ischemic retinopathy were administered an intravitreous injection of 0.1, 0.5, or 2 μg anti–VE-PTP or 2 μg IgG isotype control (n ≥12 for each). At P17, there was extensive GSA-stained retinal NV in control IgG–injected eyes and significantly less detected in eyes injected with 2 μg anti–VE-PTP. *P < 0.001 for comparison with IgG control by 1-way ANOVA with Bonferroni’s correction. Scale bar: 500 μm. (F) At P15, Rho-VEGF–transgenic mice were given an intravitreous injection of 0.5 or 2 μg anti–VE-PTP in 1 eye and a corresponding dose of control IgG in the fellow eye (n = 6 for each). At P21, there was significantly less GSA-stained subretinal NV in eyes injected with 0.5 or 2 μg anti–VE-PTP than in control IgG–injected eyes. *P = 0.01 by unpaired t test for comparison with IgG control fellow eyes. Scale bar: 100 μm. (G) Intravitreous injection of 2 μg anti–VE-PTP significantly reduced the area of choroidal NV at Bruch’s membrane rupture sites compared with control IgG. *P < 0.001 by 1-way ANOVA with Bonferroni’s correction. Scale bar: 100 μm. MW, molecular weight.