Related Experiment Video
Updated: May 20, 2026
A Mouse Model for Corneal Neovascularization by Alkali Burn
Published on: June 30, 2023
Inhibitory effect of CCR3 signal on alkali-induced corneal neovascularization
Wen-Juan Zhou1, Gao-Qin Liu, Long-Biao Li
1Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
Aim:
To investigate the effect of CC chemokine receptor 3 (CCR3) signal on corneal neovascularization (CRNV) induced by alkali burn and to explore its mechanism.
Methods:
Specific pathogen-free male BALB/C mice (aged 6-8 weeks) were randomly divided into CCR3-antagonist treated group (experimental group) and control group. CRNV was induced by alkali burn in mice. The time kinetic CCR3 expression in injured corneas was examined by reverse transcription polymerase chain reaction (RT-PCR). CCR3-antagonist (SB-328437 at different concentration of 125µg/mL, 250µg/mL, and 500µg/mL) was locally administrated after alkali injury. The formation of CRNV was assessed by CD31 corneal whole mount staining at two weeks after injury. Monocyte chemotactic protein 1 (MCP-1), monocyte chemotactic protein 3 (MCP-3) expressions in the early phase after injury were quantified and compared by RT-PCR. Macrophage intracorneal accumulation in the early phase after injury was evaluated and compared by immunohistochemistry.
Results:
Alkali injury induced the time kinetic intracorneal CCR3 expression. 500µg/mL of CCR3-antagonist treatment in the early phase but not the late phase resulted in significant impaired CRNV as compared to control group (P<0.05). CCR3-antagonist treatment in the early phase significantly reduced the intracorneal MCP-1 and MCP-3 enhancement compare to control group at day 2 and day 4 (P<0.05). Moreover, the number of intracorneal macrophage infiltration in the experimental group was reduced than those in control group at day 4 (P<0.05).
Conclusion:
CCR3 signal is involved in alkali-induced CRNV. CCR3-antagonist can inhibit alkali-induced CRNV by reducing the intracorneal MCP-1 and MCP-3 mRNA expression and the intracorneal macrophage infiltration.
Insights
CC chemokine receptor 3 (CCR3) signaling drives corneal neovascularization after alkali burns. Blocking CCR3 early significantly reduces this neovascularization by inhibiting inflammatory cell recruitment.
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Background:
- Corneal neovascularization (CRNV) is a major cause of vision impairment.
- Alkali burns are a common cause of severe ocular injury leading to CRNV.
- The role of CC chemokine receptor 3 (CCR3) in this process requires further elucidation.
Purpose of the Study:
- To investigate the impact of CCR3 signaling on alkali-induced CRNV.
- To explore the underlying mechanisms by which CCR3 influences CRNV.
Main Methods:
- Alkali-induced CRNV model in BALB/C mice.
- Time-course analysis of CCR3 expression using RT-PCR.
- Local administration of CCR3-antagonist (SB-328437) at varying concentrations.
- Assessment of CRNV by CD31 staining.
- Quantification of MCP-1 and MCP-3 expression via RT-PCR.
- Evaluation of macrophage infiltration using immunohistochemistry.
Main Results:
- Alkali injury induced time-dependent CCR3 expression in the cornea.
- Early-phase administration of 500µg/mL CCR3-antagonist significantly inhibited CRNV.
- CCR3-antagonist treatment reduced intracorneal MCP-1 and MCP-3 expression.
- Reduced macrophage infiltration was observed in the CCR3-antagonist treated group.
Conclusions:
- CCR3 signaling plays a significant role in alkali-induced corneal neovascularization.
- CCR3-antagonist effectively inhibits CRNV by modulating inflammatory mediators and macrophage recruitment.
