J Browning1, C K Wylie, G Gole. 1. School of Health Sciences, Griffith University-Gold Coast Campus, Southport, Queensland, Australia.
Abstract
PURPOSE: To describe a quantifiable model of vascular proliferation in oxygen-induced retinopathy (OIR) in the mouse. METHODS: Neonate Quackenbush mice were subjected to high-ambient oxygen (approximately 95%) for the first 5 days after birth, effecting a total inhibition of retinal vascular growth. Animals then were returned to room air, and the rates of subsequent vascular development in the plane of the retina and estimates of retinal capillary density were measured from flatmounts of ink-perfused eyes. Observations were confirmed with fluorescein isothiocyanate-lectin labeling of the peripheral vasculature. Abnormal growth of vascular sprouts into the vitreous was recorded from cross-sections. Observations in OIR were compared against those of age-matched control animals. RESULTS: The slower rate of retinal revascularization in OIR mice was quantified and compared against the normal rate. Lectin-binding studies confirmed the reliability of ink preparations. The number of vitreous sprouts in OIR peaked 8 to 10 days after animals were returned to room air (13 to 15 postnatal days). Sprouts then regressed, to disappear by postnatal day 20. In all respects, bar a slightly lower peripheral capillary density, the normal retinal vascular pattern was achieved in OIR within 15 days of exposure to room air (as opposed to the 10 days required in control mice). CONCLUSIONS: The protocol described for quantifying retinal proliferation in mouse OIR is reproduced readily, and the data recorded here will allow the effectiveness of subsequent treatments that may affect retinal vascular growth to be evaluated better.
PURPOSE: To describe a quantifiable model of vascular proliferation in oxygen-induced retinopathy (OIR) in the mouse. METHODS: Neonate Quackenbush mice were subjected to high-ambient oxygen (approximately 95%) for the first 5 days after birth, effecting a total inhibition of retinal vascular growth. Animals then were returned to room air, and the rates of subsequent vascular development in the plane of the retina and estimates of retinal capillary density were measured from flatmounts of ink-perfused eyes. Observations were confirmed with fluorescein isothiocyanate-lectin labeling of the peripheral vasculature. Abnormal growth of vascular sprouts into the vitreous was recorded from cross-sections. Observations in OIR were compared against those of age-matched control animals. RESULTS: The slower rate of retinal revascularization in OIR mice was quantified and compared against the normal rate. Lectin-binding studies confirmed the reliability of ink preparations. The number of vitreous sprouts in OIR peaked 8 to 10 days after animals were returned to room air (13 to 15 postnatal days). Sprouts then regressed, to disappear by postnatal day 20. In all respects, bar a slightly lower peripheral capillary density, the normal retinal vascular pattern was achieved in OIR within 15 days of exposure to room air (as opposed to the 10 days required in control mice). CONCLUSIONS: The protocol described for quantifying retinal proliferation in mouse OIR is reproduced readily, and the data recorded here will allow the effectiveness of subsequent treatments that may affect retinal vascular growth to be evaluated better.
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