| Retinal neovascularization is a kind of common blinding diseases, such as retinopathy of premature children, diabetic retinopathy, retinal vein occlusion and other diseases, all of which may lead to traction retinal detachment due to the formation of new blood vessel proliferation. The cause of retinal neovascularization is still not very clear and is one of the focuses of the ophthalmonogy. Retinal ischemia and hypoxia are the most important reasons for retinal neovascularization. Retinal angiogenesis induced by hypoxia is a commonly used method to reproduce the neovascular diseases for research on retinopathy of premature children [1,2]. However, the formation of hypoxia-induced retinal neovascularization is related to the used animal strains. In addition, it is reported by literature that the formation of retinal neovascularization very seldom occurs to the patients with retinitis pigmentosa and the mice with retinal degeneration mode, which brings new hope for the treatment of neovascular diseases [3]. We found that retinal degeneration fast(rdf) and rats with two patterns of spontaneous gene mutation, respectively, congenital stationary night-blindness (CSNB) [4] and retinal cone dystfunction ( RCD) [5], in adulthood only and mainly show the functional change but show no significant degenerative change in the retinal photoreceptors. To further explore the pathogenesis of retinal neovascularization, referring to literature methods [6], we prepared the models of retinal neovascularization induced by high concentrations of oxygen to neonatal animals, and the retinal neovascularization characteristics were observed in animals with three patterns of spontaneous gene mutation.Methods and materialA brood of P7 old-SD rats(6),Congenital Stablenary Night-Bliness (CSNB) rat(6),Retinal Cone Degeneration(RCD) rats(6),rdf×C57BL/6J mice(6),rdf×C57BL/6J heterozygosis mice(6) and rdf mice(6) were exposed to 80%±2% oxygen for 5 days and then to the room air for another 5 days, respectively. Age matched 6 broods of corresponding animals without high oxygen exposure was used as controls. At the P18, the hearts of all the pups were perfused with ink, and then their bilateral eye-balls were enucleated, one was used as retinal preparation to assess the change of retinal vessels, The other was used as histological section to observe and count the endothelial cell nucleus of new vessels extending from the retina into vitreous in 4um sagittal cross-sections. Newborn mice in each group in accordance with the above method of a retinal tissue sections prepare tissue sections, and the other eye's tissue sections were stained using immunostained with an anti-von Willebrand factor antibody (sigma,United States.) according to the manufacturer's instructions. See brown in the cytoplasm of vascular endothelial cells is positive.ResultsUnder normoxia raising condition, the retinal vascular net was sparse in RCD rats. The endothelial cell was sporadically observed in SD rat. After high-concentration oxygen and then normally-concentration oxygen exposure, the retinal blood vessels were constricted,occluded in six animals strains. The retinal non-perfusion area and even hemorrhage could be observed also in experimental groups, the mean number of endothelial cell nucleus extending from retina to vitreous per cross-section in SD rats, CSNB rats ,RCD rats , rdf×C57BL/6J mice, rdf×C57BL/6J heterozygosis mice and rdf mice were 24.10±2.49,38.20±10.47,68.00±3.06, 16.95±5.12,25.52±6.90,29.15±23.79, respectively. There were significant difference between control groups and experimental groups (P<0.01).Conclusion1. A high oxygen/reoxygenation can be successfully induced retinal neovascularization .2 . Oxygen-induced retinal neovascularization in neonatal rats is related to the strain . Retinal degeneration rats can be induced retinal neovascularization and severity may be relevant to the function of photoreceptor cells.3. rdf in the high oxygen / reoxygenation induced retinal neovascularization, and rd1 significantly different.
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