Related Experiment Video
Updated: Sep 23, 2026
An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Inhibition of corneal neovascularization by genetic ablation of CCR2
Balamurali K Ambati1, Antonia M Joussen, William A Kuziel
1Department of Ophthalmology, Medical College of Georgia, Augusta, 30907, USA. bambati@mail.mcg.edu
Purpose:
To determine if genetic ablation of the chemokine receptor CCR2 (involved in leukocyte and endothelial chemotaxis) inhibits the development of corneal neovascularization.
Methods:
Wild-type C57BL/6J mice, as well as species-specific counterparts with targeted homozygous disruption of the CCR2, underwent chemical and mechanical denudation of corneal and limbal epithelium. Corneas were harvested 2 weeks after injury. Neovascularization was quantified by CD31 immunostaining.
Results:
The mean percentages of neovascularized corneal area in control mice and CCR2-deficient mice 2 weeks after denudation were 58.3% and 38.8% (P = 0.047), respectively.
Conclusions:
Development of corneal neovascularization is inhibited in CCR2-deficient mice.
Insights
Genetic ablation of chemokine receptor CCR2 (CC-chemokine receptor type 2) significantly inhibited corneal neovascularization in mice. This suggests CCR2 plays a key role in the development of new blood vessels in the cornea.
Area of Science:
- Ophthalmology
- Immunology
- Vascular Biology
Background:
- Corneal neovascularization (CNV) is a significant cause of vision loss.
- Chemokine receptors, such as CCR2, are implicated in inflammatory processes and leukocyte recruitment.
- Understanding the role of specific chemokine receptors in CNV is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of the chemokine receptor CCR2 in the development of corneal neovascularization.
- To determine if genetic deletion of CCR2 affects the extent of CNV following corneal injury.
Main Methods:
- Chemical and mechanical denudation of corneal and limbal epithelium in wild-type and CCR2-deficient mice.
- Corneal tissue harvesting at 2 weeks post-injury.
- Quantification of neovascularization using CD31 immunostaining.
Main Results:
- CCR2-deficient mice exhibited significantly reduced corneal neovascularization compared to wild-type controls (38.8% vs. 58.3% neovascularized area, P = 0.047).
- Genetic ablation of CCR2 led to a marked inhibition of new blood vessel formation in the injured cornea.
Conclusions:
- The chemokine receptor CCR2 plays a critical role in promoting corneal neovascularization.
- Targeting CCR2 may represent a viable therapeutic strategy for inhibiting CNV and preserving vision.
