The following research seeks to characterize oxygen-induced retinopathy (OIR) in the rat as an animal model for retinopathy of prematurity (ROP). The ultimate goal of the study is to elucidate the mechanism by which hyperoxia causes retinal vascular degeneration. Recently, with the increasing sophistication of premature infant care, the survival of preterm infants has increased and with it the incidence of ROP. Yet, virtually nothing is known about the specific pathophysiology of this blinding disease. It has become increasingly desirable to develop an animal model which parallels the human in both retinal ontogeny and oxygen-induced retinal pathogenicity. It is of primary importance that this model constitute a reliable protocol for oxygen-induced retinopathy in which alterations in structure and function are readily measurable and in which results are predictable. To this end, four research projects are presented using the newborn ratling: 1) a careful and quantitative survey of the effects of hyperoxic conditions on the vasculature of newborn rat retinas, employing ink-perfused retinal whole mounts, fluorescein labeling, and electron microscopy; 2) a determination of any functional deficit which may occur immediately following oxygen exposure and with time post-exposure, coupled with an attempt to correlate such deficits with morphological and biochemical alterations; 3) a determination of the susceptibility of normoxic and hyperoxic ratlings to retinal lipid peroxidation - a process which has been suggested by several researchers to be causal in certain types of retinal degenerations and which may be enhanced by high atmospheric oxygen; and 4) an attempt to augment the antioxidant properties of the ratling retina by supplementation or dietary manipulation. The ability to conduct morphometrical, electrophysiological, and biochemical determinations all on the retinas of a single animal makes this a unique and powerful approach for the study of OIR.
| Watkins, William M; McCollum, Gary W; Savage, Sara R et al. (2013) Hypoxia-induced expression of VEGF splice variants and protein in four retinal cell types. Exp Eye Res 116:240-6 |
| Barnett, Joshua M; Penn, John S; Jayagopal, Ashwath (2013) Imaging of endothelial progenitor cell subpopulations in angiogenesis using quantum dot nanocrystals. Methods Mol Biol 1026:45-56 |
| Capozzi, Megan E; McCollum, Gary W; Savage, Sara R et al. (2013) Peroxisome proliferator-activated receptor-?/? regulates angiogenic cell behaviors and oxygen-induced retinopathy. Invest Ophthalmol Vis Sci 54:4197-207 |
| Rezaei, Kasra A; Toma, Hassanain S; Cai, Jiyang et al. (2011) Reduced choroidal neovascular membrane formation in cyclooxygenase-2 null mice. Invest Ophthalmol Vis Sci 52:701-7 |
| Toma, Hassanain S; Barnett, Joshua M; Penn, John S et al. (2010) Improved assessment of laser-induced choroidal neovascularization. Microvasc Res 80:295-302 |
| Barnett, Joshua M; McCollum, Gary W; Penn, John S (2010) Role of cytosolic phospholipase A(2) in retinal neovascularization. Invest Ophthalmol Vis Sci 51:1136-42 |
| Yanni, Susan E; McCollum, Gary W; Penn, John S (2010) Genetic deletion of COX-2 diminishes VEGF production in mouse retinal Müller cells. Exp Eye Res 91:34-41 |
| Yanni, Susan E; Clark, Monika L; Yang, Rong et al. (2010) The effects of nepafenac and amfenac on retinal angiogenesis. Brain Res Bull 81:310-9 |
| Recchia, Franco M; Xu, Lili; Penn, John S et al. (2010) Identification of genes and pathways involved in retinal neovascularization by microarray analysis of two animal models of retinal angiogenesis. Invest Ophthalmol Vis Sci 51:1098-105 |
| Kim, Stephen J; Toma, Hassanain S; Barnett, Joshua M et al. (2010) Ketorolac inhibits choroidal neovascularization by suppression of retinal VEGF. Exp Eye Res 91:537-43 |
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