Figure 1
Figure 1. Attenuation of pathologic angiogenesis in CYP1B1−/− mice. CYP1B1+/+ and CYP1B1−/− mice were exposed to a cycle of hyperoxia and room air (OIR). The collagen IV–stained of whole mount retinas prepared from P17 CYP1B1+/+ and CYP1B1−/− mice are shown in panels A and B, respectively (×25). The hematoxylin/PAS–stained eye sections prepared from P17 CYP1B1+/+ and CYP1B1−/− mice are shown in panels C and D, respectively (×100). The arrows indicate growth of new vascular tufts, which is significantly diminished in CYP1B1−/− mice. The number of vascular cell nuclei present on the vitreous side of the retina penetrating the inner limiting membrane was determined as described in “Methods” at P17 and presented in panel E. Data in each bar are the mean number of vascular cell nuclei in 5 eyes of 5 mice (error bars indicate SD). Please note that there is a significant decrease in the degree of retinal neovascularization in CYP1B1−/− mice compared with CYP1B1+/+ mice (n = 20, *P < .05).

Attenuation of pathologic angiogenesis in CYP1B1−/− mice. CYP1B1+/+ and CYP1B1−/− mice were exposed to a cycle of hyperoxia and room air (OIR). The collagen IV–stained of whole mount retinas prepared from P17 CYP1B1+/+ and CYP1B1−/− mice are shown in panels A and B, respectively (×25). The hematoxylin/PAS–stained eye sections prepared from P17 CYP1B1+/+ and CYP1B1−/− mice are shown in panels C and D, respectively (×100). The arrows indicate growth of new vascular tufts, which is significantly diminished in CYP1B1−/− mice. The number of vascular cell nuclei present on the vitreous side of the retina penetrating the inner limiting membrane was determined as described in “Methods” at P17 and presented in panel E. Data in each bar are the mean number of vascular cell nuclei in 5 eyes of 5 mice (error bars indicate SD). Please note that there is a significant decrease in the degree of retinal neovascularization in CYP1B1−/− mice compared with CYP1B1+/+ mice (n = 20, *P < .05).

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