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Updated: Apr 28, 2026
An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
[Inhibited experimental mouse corneal neovascularization by CCR3 antagonist]
Gaoqin Liu1, Xuefei He1, Wenjuan Zhou1
1Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Objective:
To explore the effect of CCR3 antagonist on the development of experimental corneal neovascularization.
Methods:
Mouse corneas were burned by NaOH to induce corneal neovascularization.Fifty four clean male BABL/c mice aged 7-8 weeks were divided into control group, CCR3 antagonist group and VEGF antibody positive group according to randomized number table. The gene expression of CCR3 and its ligand eotaxin in burned corneas was examined by Real-time PCR. CCR3 antagonist was locally administrated after alkali injury and the formation of corneal neovascular 2 weeks after injury was examined using a digital camera linked to a slit lamp microscope and corneal whole mount staining with CD31. The mRNA and protein expression of chemokines in burned corneas was detected by Real-time PCR and western blot.
Results:
Compared to control group, CCR3 antagonist treated mice resulted in significantly decreased corneal neovascularization. The related CNV area was 0.51 ± 0.03 in the CCR3 antagonist group, and that in the control group was 0.77 ± 0.15, with significant difference between them (t = 12.91, P = 0.00).Western blot detection did not show significant difference of VEGF protein expression between two groups.Expression level of VEGF in the CCR3 antagonist group was 0.91 ± 0.24, and that in the control group was 1.15 ± 0.30, showing no significant difference (t = 1.08, P = 0.34).
Conclusions:
Alkali-induced corneal neovascularization was inhibited by CCR3 antagonist. The mechanism that CCR3 pathway plays an important role in corneal neovascularization needs further exploration.
Insights
CCR3 antagonist significantly inhibited alkali-induced corneal neovascularization in mice. This suggests the CCR3 pathway is crucial for neovascularization development, warranting further investigation.
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Context:
- Corneal neovascularization (CNV) is a pathological process.
- It can lead to vision impairment.
- Understanding its underlying mechanisms is critical for developing effective treatments.
Purpose:
- To investigate the therapeutic potential of a CCR3 antagonist.
- To explore the role of the CCR3 pathway in experimental corneal neovascularization.
Summary:
- Alkali burns induced experimental corneal neovascularization in mice.
- Mice treated with a CCR3 antagonist showed significantly reduced CNV.
- VEGF protein expression was not significantly altered between groups.
Impact:
- CCR3 antagonist demonstrates efficacy in reducing experimental CNV.
- Highlights the CCR3 pathway as a potential therapeutic target for corneal neovascularization.
- Suggests novel treatment strategies for vision-threatening ocular conditions.
