The Role Of Erythropoietin In Neovascular Glaucoma

Objective:The purpose of this study was to determine the vitreous and aqueous levels of erythropoietin(EPO)and vascular endothelial growth factor(VEGF)in patients with neovascular glaucoma.Explore the effects of EPO and VEGF on neovascularization in vitro and valuate the inhibitory effect of soluble erythropoietin receptor(sEPOR)on oxygen-induced retinal neovascularization in mice.Methods:1.A sandwich enzyme-linked immunosorbent assay was used to detect the vitreous and aqueous EPO and VEGF levels in glaucoma patients in our hospital from June 2014 to October 20142.Explore the effects of EPO and VEGF on vascular-like and capillary-like structure formations in human umbilical vein endothelial cells(HUVECs)3.The mouse model of oxygen-induced retinopathy was used to observe the retinal vascular changes after FITC-dextran perfusion.The inhibitory effect of sEPOR on EPO and VEGF expressions was evaluated by real-time PCR and western blot.Results:1.The average levels of vitreous and aqueous EPO and VEGF in patients with neovascular glaucoma were significeantly higher than that in control group.2.Compared with control,EPO and VEGF induced the vascular-like and capillary-like structure formations in HUVECs(P<0.01).10 IU/ml and 100 IU/ml EPO as well as 10ng/ml VEGF significantly induced the proliferation of HUVECs(P<0.01).3.sEPOR effectively inhibited the neovascularization in mouse model of oxygen-induced retinopathy and-down regulated the expression of EPO and VEGF in a dose-dependent manner.Conclusion:1.Both EPO and VEGF played an important role in neovascular glaucoma.2.EPO and VEGF promoted the neovascularization by inducing the proliferation of EPCs and the vascular-like formation.3.sEPOR effectively inhibited the neovascularization in mouse model of oxygen-induced retinopathy and-down-regulated the expressions of EPO and VEGF.