Effect of Oxygen on Photoreceptor Degeneration in Retinal Degeneration Mice

ABSTRACT

There is still no effective treatment for retinal degenerative diseases, in which the loss of photoreceptor cells causes visual loss and eventually blindness. Despite the current studies show that intraocular injection of basic fibrobalst growth factor rescues damaged and dystrophic rat photoreceptor in transgenic animal, there is a few evidence that endogenous neurotrophic factor promotes photorecptor cell survival in retina. In the present study, retinal degeneration (rd)neonate mice were exposed to hyperoixa for 5 days, and then were returned to room air, which was presumed to cause relative hypoxia of nonperfused retina, producing a neovascular response. Using this model, we investigated the effect of relative hypoxia on degenerative process in rd mice. As a control, rd neonate mice were remained at room air from birth. At the postnatal 10, 12, 14, 16, 18 and 21 days, the ratio of total retinal thickness and outer nuclear layer (ONL)thickness, and neovascularization of experimental right eyes were compared with those of control. Extent of vascularization of experimental left eyes was compared with that of left eyes in control group. In rd mice, extraretinal neovascularization was observed in 62%of 93 eyes of the experimental group exposed to hyperoxia. Extent of vascularization in experimental group was smaller than that of in control. There was an oxygen-induced modulation of rates of death in experimental group, where-as the death of photoreceptor progressed in control group. In experimental group, the ratio of total retinal thickness and ONL thickness was higher than that of in control group at 18 and 21 days of age. These results suggest that the relative hypoxia in the rd mice may have rescue effect on photoreceptor in rd mice.