Objective To investigate the inhibitory effects of FGFR1-Fc on the proliferation,migration and angiogenesis of human retinal microvascular endothelial cell(HRCEC)stimulated by bFGF.To validate the inhibitory effects in oxygen-induced retinal neovascularization(OIR)mice model,and preliminarily study the synergistic effect of FGFR1-Fc and anti-VEGF drugs.Methods HRCEC were cultured in vitro and cells were treated with bFGF and different concentrations of FGFR1-FC.MTT assay was used to determine cell activity,scratch assay was used to detect cell migration ability,flow cytometry was used to detect cell cycle,and Western blotting was used to ascertain protein expression levels.OIR mice were used as animal models to observe the state of retinal blood vessels and calculate the area of retinal non-perfusion area.The extent of neovascularization was evaluated by counting the number of intravitreal vascular nuclei,which were defined as the nuclei of cells that extended beyond the inner limiting membrane of the retina into the vitreous vio Hematoxylin-eosin staining(HE).Results FGFR1-Fc inhibited bFGF-stimulated HRCEC proliferation,and suppressed p38,ERK1/2 and AKT phosphorylation,thus inhibitd the cell proliferation stimulated by bFGF.FGFR1-Fc inhibited cell cycle progression and blocked cell proliferation in G0/G1 phase.FGFR1-Fc inhibited bFGF-stimulated HRCEC migration,and FGFR1-Fc might down-regulate the expression of migration-related proteins by inhibiting the activation level of STAT3,and ultimately inhibited angiogenesis.FGFR1-Fc and Razumab could inhibit retinal neovascularization,and had a certain synergistic effect.Conclusion FGFR1-Fc inhibits bFGF-stimulated HRCEC proliferation,migration,and angiogenesis.FGFR1-Fc and anti-VEGF drugs have a synergistic effect.
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