AIM:To examine the expression of survivin and vascular endothelial growth factor(VEGF) during the development of retinal neovascularization(NV) in a mouse model.· METHODS:A well-characterized murine model of retinal NV was used to study the expression of survivin and VEGF.NV of the retina was induced in mice by exposure to 75% O2 from postnatal day P7 to P12,followed by return to room air from P12 to P17.Expression of survivin and VEGF protein was analyzed by Immunohistochemistry.In addition,mouse model of proliferative retinopathy was analyzed by retinal fluorescein angiography and quantification analysis.· RESULTS:The normal mice had both superfiekal and deep vascular layers that extended from the optic nerve to the periphery.In intraocular pressure(IOP) mice were characterized by represent a typical pattern of pathological retinal NV.There are less or little nuclei of new vessels vascular endothelial cell breaking through the inner retinal than in retinopathy of prematurity(ROP) mice,large clusters of blood vessels were adherent to the internal limiting membrane(ILM)(0.27±0.20 vs 23.38±1.027,t =9.454,P < 0.001).During the angiogenic period from P13 to P17,survivin and VEGF protein expression increased in experimental retinas compared with control samples(2.56±0.46 vs 3.34±0.40,t =17.43,P <0.01:2.18±0.75 vs 4.34±0.25,t =19.61,P <0.01).Protein levels of VEGF and survivn has significantly positive correlation(P <0.05,r =0.411).· CONCLUSION:Correlation was made at the protein levels of survivin expression compared with that of VEGF in a murine model of retinal NV,which suggests a temporal role for survivin and VEGF in new vessel formation in response to hypoxic stimulation. AIM: To examine the expression of survivin and vascular endothelial growth factor (VEGF) during the development of retinal neovascularization (NV) in a mouse model. METHODS: A well-characterized murine model of retinal NV was used to study the expression of survivin and VEGF. NV of the retina was induced in mice by exposure to 75% O2 from postnatal day P7 to P12, followed by return to room air from P12 to P17. Expression of survivin and VEGF protein was analyzed by Immunohistochemistry. In addition, mouse model of proliferative retinopathy was analyzed by retinal fluorescein angiography and quantification analysis. RESULTS: The normal mice had both superfiekal and deep vascular layers that extended from the optic nerve to the periphery. In intraocular pressure (IOP) mice were characterized by represent a typical pattern of pathological retinal NV. There are less or little nuclei of new vessels vascular endothelial cell breaking through the inner retinal than in retinopathy of prematurity (ROP) m ice, large clusters of blood vessels were adherent to the internal limiting membrane (ILM) (0.27 ± 0.20 vs 23.38 ± 1.027, t = 9.454, P <0.001). in experimental retinas compared with control samples (2.56 ± 0.46 vs. 3.34 ± 0.40, t = 17.43, P <0.01: 2.18 ± 0.75 vs. 4.34 ± 0.25, t = 19.61, P <0.01) correlation (P <0.05, r = 0.411). CONCLUSION: Correlation was made at the protein levels of survivin expression compared with that of VEGF in a murine model of retinal NV, which suggests a temporal role for survivin and VEGF in new vessel formation in response to hypoxic stimulation.