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Updated: Apr 12, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Intravitreal inhibition of complement C5a reduces choroidal neovascularization in mice
Claudia Brockmann1, Tobias Brockmann2, Sabrina Dege2
1Department of Ophthalmology, Charité - University Medicine Berlin, Augustenburger Platz 1, 13353, Berlin, Germany. claudia.brockmann@charite.de.
Purpose:
To investigate the influence of complement component C5a inhibition on laser-induced choroidal neovascularization (CNV) in mice using a C5a specific L-aptamer.
Methods:
In C57BL/6 J mice CNV was induced by argon-laser, C5a-inhibitor (NOX-D20) was intravitreally injected in three concentrations: 0.3, 3.0, and 30 mg/ml. The unPEGylated derivate (NOX-D20001) was applied at 3.0 mg/ml; the vehicle (5 % glucose) was injected in controls. Vascular leakage was evaluated using fluorescence angiography, CNV area was examined immunohistochemically. Activated immune cells surrounding the CNV lesion and potential cytotoxicity were analyzed.
Results:
Compared to controls, CNV areas were significantly reduced after NOX-D20 injection at a concentration of 0.3 and 3.0 mg/ml (p = 0.042; p = 0.016). NOX-D20001 significantly decreased CNV leakage but not the area (p = 0.007; p = 0.276). At a concentration of 30 mg/ml, NOX-D20 did not reveal significant effects on vascular leakage or CNV area (p = 0.624; p = 0.121). The amount of CD11b positive cells was significantly reduced after treatment with 0.3 and 3.0 mg/ml NOX-D20 (p = 0.027; p = 0.002). No adverse glial cell proliferation or increased apoptosis were observed at effective dosages.
Conclusions:
Our findings demonstrate that the targeted inhibition of complement component C5a reduces vascular leakage and neovascular area in laser-induced CNV in mice. NOX-D20 was proven to be an effective and safe agent that might be considered as a therapeutic candidate for CNV treatment. The deficiency of activated immune cells highlights promising new aspects in the pathology of choroidal neovascularization, and warrants further investigations.
Insights
Targeted inhibition of complement component C5a with NOX-D20 significantly reduced vascular leakage and choroidal neovascularization (CNV) areas in mice. This safe and effective agent shows therapeutic potential for CNV treatment.
Area of Science:
- Ophthalmology
- Immunology
- Vascular Biology
Background:
- Choroidal neovascularization (CNV) is a leading cause of vision loss.
- The complement system, particularly C5a, plays a role in CNV pathogenesis.
- Inhibiting C5a may offer a novel therapeutic strategy for CNV.
Purpose of the Study:
- To evaluate the efficacy of C5a inhibition using a specific L-aptamer (NOX-D20) in a mouse model of laser-induced CNV.
- To assess the impact of NOX-D20 on vascular leakage, CNV area, and immune cell activation.
Main Methods:
- CNV was induced in C57BL/6 J mice using argon laser photocoagulation.
- Intravitreal injections of NOX-D20 at varying concentrations (0.3, 3.0, 30 mg/ml) or vehicle were administered.
- Vascular leakage was assessed via fluorescein angiography, and CNV area was quantified immunohistochemically.
Main Results:
- NOX-D20 significantly reduced CNV area at 0.3 and 3.0 mg/ml concentrations (p<0.05).
- Vascular leakage was decreased by NOX-D20001 (unPEGylated derivate) but not CNV area (p<0.007).
- Treatment with effective NOX-D20 doses significantly reduced CD11b positive immune cells without observed cytotoxicity.
Conclusions:
- Targeted C5a inhibition effectively reduces vascular leakage and CNV area in a mouse model.
- NOX-D20 demonstrates safety and efficacy, positioning it as a potential therapeutic candidate for CNV.
- The reduction in activated immune cells suggests novel insights into CNV pathology requiring further research.
