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• W54193075 abstract "Retinopathy of prematurity (ROP) is a disease process that involves abnormal retinal neovascularization in low birth weight premature infants and it is usually associated with oxygen supplementation. It has been hypothesized that high concentration oxygen which is used to keep the premature babies alive causes vascular damage leading to retinal hypoxia. The hypoxic retina is thought to produce angiogenic molecules such as vascular endothelial growth factor (VEGF) which stimulate overgrowth of retinal vessels leading to retinopathy. Using a mouse model of oxygen-induced retinopathy (OIR), the effect of increased inspired oxygen concentration (FiO2j) on neonatal retinal vessel architecture was examined in fluorescein and ink perfusion experiments. The temporal and spatial expression of the VEGF gene during the development of normal retinal vascularization and oxygen-induced retinopathy was then studied. To investigate the role of oxygen regulation in the expression of VEGF gene, the oxygen status in the retina was examined using a marker to detect the hypoxic cells in the retina. The first series of experiments show that the retinal artery, vein and capillary bed exhibit a vasoconstrictive response after exposure to high concentration oxygen in neonatal mice. The extent of retinal artery constriction appeared to be independent of the concentration of inspired oxygen. Peripheral capillary ablation was more marked in animals exposed to the high concentration of oxygen (95%) suggesting an additional effect of oxygen on the capillary bed. The expression of VEGF mRNA and protein was analysed during the development of normal retinal vascularization and oxygen-induced neovascularization. VEGF mRNA was localized at the inner nuclear layer and ganglion cell layer. In the inner nuclear cell layer VEGF mRNA was expressed by retinal Muller cells. VEGF protein was found around the retinal vessels, including hyaloid vessels, fi-om the nerve fiber layer of the retina (close to the incident light surface of the retina) to the inner nuclear layer where the new vessels were developing. Both VEGF protein and mRNA were found in macrophages located in the vitreous, ganglion cell layer and inner nuclear cell layer. VEGF mRNA and protein level decreased following a period of hyperoxia exposure compared with the control group and increased on return to room air reaching a peak at 3 days (VEGF mRNA) and 5 days (VEGF protein). RT-PCR revealed the presence in the retina of four VEGF RNA constructs in the control group. Two strong PCR bands corresponded to mRNA for VEGF 120 and VEGF 164 and one faint band corresponded to VEGF188 mRNA. The fourth band was possibly VEGF206 mRNA according to the size of PCR product. In the oxygen-treated group, two strong bands were generated corresponding to VEGF120 and VEGF164 mRNA while VEGF188 and VEGF206 niRNA were not detectable. Hypoxia in the retina was examined using 7-[4'-(2-nitroimidazol-lyl) butyl]theophylline (NITP) as a hypoxic marker. The results showed that during development of normal retinal vasculature the hypoxic cells were present at a very low level. In the adult retina the marker for hypoxia was hardly detectable. After 72 hr exposure to 95% oxygen tension the number of hypoxic cells increased. After 5 days exposure to 95% oxygen the hypoxic area in the retina increased about 8 fold compared to controls. In the oxygen treated groups, after 5 days return to room air, the hypoxic area reached a peak and about 16 fold compared to controls. The hypoxic area then decreased in size but remained at a higher level than the control group. In summary, vasoconstriction and obliteration of vessels in the retina following high oxygen exposure leads to retinal neovascularization after animals are returned to room air. VEGF is expressed during normal retinal vascular development. During the development of oxygen-induced retinopathy, there is overexpression of VEGF and an increase in the area of hypoxia in the retina. The findings support the hypothesis that VEGF is important for retinal neovascularization and is upregulated following retinal hypoxia." @default.
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• W54193075 date "2003-01-01" @default.
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• W54193075 title "The expression of the VEGF gene in a mouse model of oxygen-induced retinopathy" @default.
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