Anti-angiogenic and anti-inflammatory effects of CD200-CD200R1 axis in oxygen-induced retinopathy mice model
Related Experiment Video
Updated: Jan 20, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Yaguang Hu1, Ting Wei1, Shan Gao1
1Department of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, China.
Objective:
In this study, the expression changes and the potential effects of CD200 and its receptors during the process of retinal neovascularization (RNV) development had been detected, using a classic oxygen-induced retinopathy (OIR) mice model and CD200Fc (a CD200R1 agonist) intravitreal injection.
Materials And Methods:
7 day postnatal (P7) C57BL/6J mice were raised in hyperoxia incubators with 75±2% oxygen for 5 days, and returned to room air at P12. All animals were subdivided into three groups: normoxia control, OIR, and OIR+CD200Fc group. The mice of OIR+CD200Fc group were intravitreal injected with CD200Fc (2μg/μL, 0.5μL) at P12. Retinas and vitreous samples were harvested at P17. The expression and localization of CD200 and its receptors were analyzed by Western blot, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and retinal whole-mount immunofluorescence. To investigate the effects of CD200Fc treatment, vascular endothelial growth factor (VEGF)-A, platelet-derived growth factor (PDGF)-BB, pro-inflammatory cytokines, NV area, and microglial activation were detected respectively.
Results:
In OIR group, both protein and RNA levels of CD200 and CD200R1 were significantly up-regulated. The increased CD200 and CD200R1 were co-localized with Alex594-labeled Griffonia simplicifolia isolectin B4 (IB4) on vascular endothelial cells in NV area of OIR samples, and CD200R1 was co-expressed with ionized calcium-bind adapter molecule 1 (iba1) on microglia in OIR samples at the same time. CD200Fc intravitreal injection could significantly reduce the release of VEGF-A, PDGF-BB, and pro-inflammatory cytokines; shrink the NV area; and inhibit the activation of microglia in OIR mice.
Conclusion:
These findings suggested that the up-regulation of CD200 and CD200R1 was closely related to RNV development, and the antiangiogenic effects of CD200Fc in OIR model might be realized by inhibition of inflammatory response and microglia activation. The results may provide a new therapeutic target for RNV diseases.
Insights
CD200 and its receptors are upregulated in retinal neovascularization (RNV). Treatment with CD200Fc reduces RNV by inhibiting inflammation and microglia activation, suggesting a new therapeutic target for RNV diseases.
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Background:
- Retinal neovascularization (RNV) is a major cause of vision loss.
- The role of CD200 and its receptors in RNV pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the expression of CD200 and its receptors during RNV development.
- To evaluate the therapeutic potential of CD200Fc in an oxygen-induced retinopathy (OIR) mouse model.
Main Methods:
- An OIR mouse model was established.
- CD200Fc was administered via intravitreal injection.
- Expression analysis of CD200, CD200R1, VEGF-A, PDGF-BB, and inflammatory cytokines was performed using Western blot, qRT-PCR, and ELISA.
- Retinal neovascularization and microglial activation were assessed.
Main Results:
- CD200 and CD200R1 expression were significantly upregulated in the OIR model.
- CD200Fc treatment reduced VEGF-A, PDGF-BB, and pro-inflammatory cytokine levels.
- CD200Fc administration decreased the neovascularization area and inhibited microglial activation.
Conclusions:
- Upregulation of CD200 and CD200R1 is associated with RNV development.
- CD200Fc exhibits anti-angiogenic effects by inhibiting inflammation and microglia activation.
- CD200Fc represents a potential therapeutic strategy for RNV diseases.
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