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Updated: May 22, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Role of unc5b in retinal neovascularization in mice with oxygen-induced retinopathy
Dan Liu1, Xiao-Bo Xia, Xue-Liang Xu
1Department of Ophthalmology, Xiangya Hospital of the Central South University, Changsha 410013, Hunan Province, China.
Aim:
To explore the role of unc5b in retinal neovascularization in murine oxygen-induced retinopathy (OIR).
Methods:
On postnatal 7(P7), C57BL/6J mice were exposed to 75%±2% oxygen for 5 days. On postnatal 12(P12), the mice were brought back to the room air (21% oxygen) to induce retinal neovascularization. Western blot analysis was performed to examine the temporal expression of unc5b in murine retinas. Double staining for unc5b and isolectin B4 were employed to determine the location of unc5b in murine retinas. The effect of unc5b on retinal neovascularization was evaluated by intravitreal injection of unc5b-FC in mice with OIR. Retinal neovascularization was measured by counting neovascular cell nuclei above the internal limiting membrane and by angiography of flat-mounted retinas perfused with fluorescein dextran.
Results:
Compared to age-matched normal mice, the expression of unc5b was significantly increased in retinas of OIR mice on P17 and P21. Unc5b was apparently expressed in retinal vessels of OIR while being negative in normal retinal vessels. Retinal neovascularization in eyes injected with unc5b-FC was significantly reduced.
Conclusion:
Unc5b-FC can effectively inhibit retinal neovascularization induced by OIR. It may serve as a powerful and novel therapy for ischemia-induced retinal disease.
Insights
Unc5b protein is elevated in oxygen-induced retinopathy (OIR) and inhibiting it with Unc5b-FC significantly reduces retinal neovascularization, suggesting a potential therapy for ischemic retinal diseases.
Area of Science:
- Ophthalmology
- Molecular Biology
- Vascular Biology
Background:
- Retinal neovascularization is a hallmark of ischemic retinopathies.
- Understanding the molecular mechanisms driving aberrant blood vessel growth is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of Unc5b in the pathogenesis of oxygen-induced retinopathy (OIR) in mice.
- To evaluate the therapeutic potential of targeting Unc5b in OIR.
Main Methods:
- Murine model of oxygen-induced retinopathy (OIR) was established.
- Temporal expression and localization of Unc5b in retinal vessels were analyzed using Western blot and double staining.
- The effect of Unc5b inhibition via intravitreal injection of Unc5b-FC on retinal neovascularization was assessed.
Main Results:
- Unc5b expression was significantly upregulated in the retinas of OIR mice compared to controls.
- Unc5b was predominantly localized to retinal vessels in OIR, but not in normal retinas.
- Intravitreal injection of Unc5b-FC markedly reduced retinal neovascularization in OIR mice.
Conclusions:
- Unc5b plays a significant role in promoting retinal neovascularization in OIR.
- Unc5b-FC demonstrates potent inhibitory effects on OIR-induced neovascularization.
- Unc5b-FC represents a promising novel therapeutic strategy for ischemic retinal diseases.
