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R.S. Charrad, R. Archer, J.D. Ash; Age–Dependent Severity of Oxygen–Induced Ischemic Retinopathy in Mice Is Associated With a Higher Sustained Expression of VEGF . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3263.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:The greatest risk factor for developing blindness in premature infants is the developmental age and size of the infant at birth. The most premature infants have the highest risk of disease. To study the mechanisms for the age–dependent severity of retinopathy of prematurity, we have previously developed a mouse model of oxygen–induced retinopathy in early neonatal mice. Our younger model has more severe retinopathy complications than the well established mouse model developed by Lois Smith. One hundred percent of mice develop severe retinopathy, and unlike the Smith model, they do not spontaneously recover. Our purpose was to determine the mechanisms for increased disease severity, and the failure to recover. Methods: For our severe model, mice are exposed to oxygen from P2 to P9, and for the Smith model from P7 to P13. Vascularization of the retina was studied using flatmounted retinas and lectin staining. VEGF expression was measured by ELISA and Western blots. Results: In the Smith model, VEGF expression was elevated 4 days after return to room air, but decreased as the vasculature damage was repaired. However, in the severe model, VEGF expression remained elevated and the vascular damage did not repair. Conclusions: These results suggest that if VEGF levels are high, but not too high, vascular damage can be repaired in mice, but that if VEGF levels are excessively high, the angiogenic response is less effective at generating healthy blood vessels and results in the formation of pathological vasculature structures that are not effective at reducing ischemia.
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