AIM: To investigate the role of CCR7/p-ERK1/2/VEGF signaling in the mouse model of oxygen-induced retinopathy(OIR). METHODS: Neonatal C57BL/6J mice were evenly randomized into four groups: normoxia, OIR, OIR control(treated with scramble si RNA), and OIR treated(treated with CCR7 siRNA). Normoxia group was not specially handled. Postnatal day 7(P7) mice in the OIR group were exposed to 75%±5% oxygen for 5d(P7-P12) and then maintained under normoxic conditions for 5d(P12-P17). Mice in the OIR control and OIR treated groups were given injections of scramble or CCR7 si RNA plasmid on P12 before returning to normoxic conditions for 5d(P12-P17). Retina samples were collected from all mice on P17, stained with adenosine diphosphatase(ADPase), and retinal neovascularization(RNV) was assessed. Retinas were also stained with hematoxylin and eosin(H&E) for RNV quantitation. The distribution and expression of CCR7, p-ERK1/2 and vascular endothelial growth factor(VEGF) were assessed via immunohistochemistry, Western blot, and quantitative real-time polymerase chain reaction(q RT-PCR). RESULTS: High oxygen promoted retinal neovascularization(P<0.05) and increased the number of endothelial nuclei in new vessels extending from the retina to the vitreous body; CCR7 promoted this process(P<0.05). CCR7 and VEGF m RNA were expressed at higher levels in the OIR and OIR control groups than in the normoxia and OIR treated groups. CCR7, p-ERK1/2, and VEGF protein were expressed in the retinas of mice in the OIR and OIR control groups. Intravitreal injection of CCR7 si RNA significantly reduced CCR7, p-ERK1/2, and VEGF expression in the OIR mouse model(all P<0.05). CCR7 significantly enhancedthe neovascularization and non-perfusion areas in the OIR group(P<0.05). CCR7 si RNA significantly reduced levels of p-ERK1/2 and VEGF as compared to OIR controls(P<0.05). CONCLUSION: These results suggest that CCR7/p-ERK 1/2/VEGF signaling plays an important role in OIR. CCR7 may be a potential target for the prevention and treatment of retinopathy of prematurity. AIM: To investigate the role of CCR7 / p-ERK1 / 2 / VEGF signaling in the mouse model of oxygen-induced retinopathy (OIR). METHODS: Neonatal C57BL / 6J mice were evenly randomized into four groups: normoxia, OIR, OIR control Normoxia group was not carefully handled. Postnatal day 7 (P7) mice in the OIR group were exposed to 75% ± 5% oxygen for 5d (P7- P12) and then maintained under normoxic conditions for 5d (P12-P17). Mice in the OIR control and OIR treated groups were given injections of scramble or CCR7 si RNA plasmid on P12 before returning to normoxic conditions for 5d (P12-P17). Retina samples were collected from all mice on P17, stained with adenosine diphosphatase (ADPase), and retinal neovascularization (RNV) was assessed. Retinas were also stained with hematoxylin and eosin (H & E) for RNV quantitation. The distribution and expression of CCR7, p -ERK1 / 2 and vascular endothelial growth factor (VEGF) were assessed via immunohis RESULTS: High oxygen promoted retinal neovascularization (P <0.05) and increased the number of endothelial nuclei in new vessels extending from the retina to the vitreous body (tRT-PCR) ; CCR7 and VEGF m RNA were expressed at higher levels in the OIR and OIR control groups than in the normoxia and OIR treated groups. CCR7, p-ERK1 / 2, and VEGF protein were expressed in the retinas of mice in the OIR and OIR control groups. Intravitreal injection of CCR7 si RNA significantly reduced CCR7, p-ERK1 / 2, and VEGF expression in the OIR mouse model (all P <0.05). CCR7 significantly enhanced the neovascularization and non CCL7 si RNA significantly reduced levels of p-ERK1 / 2 and VEGF as compared to OIR controls (P <0.05). CONCLUSION: These results suggest that CCR7 / p-ERK 1 / 2 / VEGF signaling plays an important role in OIR. CCR7 may be a potential targe tfor the prevention and treatment of retinopathy of prematurity.