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J. U. Sung, B. Oveson, Y.-J. Jo, J. Shen, T. Sedlak, S. Blackshaw, S. H. Snyder, P. A. Campochiaro; Heme Oxygenase Pathway in Retinal Degenerations. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4488.
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To evaluate the role of the heme oxygenase degradation pathway and its end product, bilirubin in retinal degenerations.
Localization in ocular tissues of heme oxygenase-1, heme oxygenase-2, and biliverdin reductase expression were performed using in situ hybridization. Heme oxygenase-2 knockout mice and two murine models of oxidative damage were employed to evaluate the role of the heme oxygenase pathway - paraquat-induced retinal degeneration and light-induced retinal degeneration. Intravitreal injections of bilirubin were performed to evaluate its effect on these models of retinal degeneration.
Heme oxygenase-1, heme oxygenase-2, and biliverdin reductase expression were found in the outer nuclear layer of the retina, retinal pigmented epithelium, cornea, and extraocular muscles. Heme oygenase-1 was also found in lens tissue. In heme oxygenase-2 knockout mice, a-wave amplitudes of electroretinograms were markedly decreased compared to wild-type mice in paraquat-induced oxidative damage models. In both the paraquat-induced and light-damage retinal degeneration models, mice injected with intravitreal bilirubin showed less of a decrease in the a- and b-wave amplitudes compared with control eyes.
There is expression of the heme degradation pathway in ocular tissues including the retina and retinal pigmented epithelium. In the heme oxygenase-2 knockout mouse, the retinal cones may be more susceptible to oxidative damage due to paraquat. Bilirubin may provide a neuroprotective effect against oxidative damage in the paraquat-induced and light-induced retinal degeneration models.
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