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Updated: Apr 26, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Blockage of tissue factor ameliorates the lesion of laser-induced choroidal neovascularization in mice
Li Wang1, Zhongkai Yang2, Ying Yu1
1Eye Institute, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong 226001, Jiangsu, China.
Abstract:
Choroidal neovascularization (CNV) occurs as a result of age-related macular degeneration (AMD) and causes severe vision loss among elderly patients. High expression of tissue factor (TF) was found in the retinas of AMD patients. In this study, we used anti-TF monoclonal antibody to test the effect of the TF blockage on experimental CNV induced by laser photocoagulation of retina in mice. Anti-TF monoclonal antibody or vehicle was administered intravitreally at day 1, 2 or 3 after laser application. We found that TF expression increased, and reached the peak at the 3rd week after the after laser application. Anti-TF monoclonal antibody can predominantly decrease the expression of TF, VEGF and F4/80, and reduced the area of CNV. Anti-TF monoclonal antibody also decreased incidence of CNV and leakage area. There were no pathological changes in the liver, heart, brain or kidney tissue. We conclude that TF plays an important role in CNV and anti-TF monoclonal antibody significantly decreases CNV in mouse model and anti-TF monoclonal antibody may have therapeutic potential in AMD.
Insights
Blocking tissue factor (TF) with an anti-TF monoclonal antibody significantly reduced choroidal neovascularization (CNV) in a mouse model. This suggests anti-TF therapy may hold promise for treating age-related macular degeneration (AMD).
Area of Science:
- Ophthalmology
- Immunology
- Vascular Biology
Background:
- Choroidal neovascularization (CNV) is a major cause of vision loss in age-related macular degeneration (AMD).
- Elevated tissue factor (TF) expression is observed in the retinas of AMD patients.
Purpose of the Study:
- To investigate the therapeutic potential of blocking TF using an anti-TF monoclonal antibody in a mouse model of laser-induced CNV.
Main Methods:
- Experimental CNV was induced by laser photocoagulation in mice.
- Anti-TF monoclonal antibody or vehicle was administered intravitreally at different time points post-laser.
- TF expression levels and CNV parameters were assessed.
Main Results:
- TF expression peaked at 3 weeks post-laser and was reduced by anti-TF antibody treatment.
- Anti-TF antibody treatment decreased TF, VEGF, and F4/80 expression.
- CNV area, incidence, and leakage were significantly reduced by anti-TF antibody.
- No significant adverse pathological changes were observed in major organs.
Conclusions:
- TF plays a critical role in the pathogenesis of CNV.
- Anti-TF monoclonal antibody demonstrates significant efficacy in reducing CNV in a preclinical model.
- Anti-TF antibody therapy represents a potential therapeutic strategy for AMD.
