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. Author manuscript; available in PMC: 2010 Jul 16.
Published in final edited form as: J Cell Physiol. 2009 Jun;219(3):544–552. doi: 10.1002/jcp.21698

Figure 1. Mice deficient in superoxide dismutase 1 (Sod1−/−) show excessive amounts of VEGF-induced subretinal neovascularization compared to Sod1+/− or Sod1+/+ mice.

Figure 1

Rho/VEGF (RhoVegf+/−) transgenic mice that express VEGF in photoreceptors under control of the rhodopsin promoter were crossed with Sod1−/− and Sod1+/−RhoVegf+/− mice were crossed to obtain Sod1+/−RhoVegf+/+ mice which were crossed with Sod1+/−RhoVegf−/− mice to obtain several litters. At P21, the mice were genotyped and perfused with fluorescein-labeled dextran. The number of neovascular lesions and the total area of neovascularization on the outer surface of the retina were measured on retinal flat mounts by image analysis and afterward the genotype was unmasked. Sod1+/+RhoVegf+/− (A) and Sod1+/−RhoVegf+/− (B) appeared to have less neovascularization than Sod1−/−RhoVegf+/− mice (C). The neovascular tufts are indicated by arrows, but at this relatively low magnification the retinal vessels are seen in the background. At higher magnification (D), the narrow depth of field eliminates the background and the buds of neovascularization on the outer surface of the retina are seen more clearly (arrows) as is a feeder vessel (arrowhead) to the superior-most lesion. Image analysis showed that Sod1−/−RhoVegf+/− mice (n=10) had significantly greater mean (±SEM) number of neovascular lesions (E) and greater mean (±SEM) total area of neovascularization per retina (F) than Sod1+/+RhoVegf+/− (n=6) or Sod1+/−RhoVegf+/− (n=10).

*p=0.0015; **p=0.0007 by ANOVA with Dunnett’s correction for multiple comparisons. Bar = 100 μm