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Updated: May 27, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Endogenous osteopontin involvement in laser-induced choroidal neovascularization in mice
Norihito Fujita1, Shuko Fujita, Nahoko Ogata
1Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan. norihito@wakayama-med.ac.jp
Purpose:
To evaluate the effects of the lack of osteopontin (OPN) and the administration of anti-OPN antibody on inflammation and vascular endothelial growth factor (VEGF) expression in choroidal tissue and on the development of choroidal neovascularization (CNV) after retinal photocoagulation in mice.
Methods:
CNV was induced in one eye each of 20 C57BL/6-background OPN-deficient mice or 20 wild-type littermates. In another series of experiments, CNV was induced in 40 C57BL/6 mice treated with intraperitoneal administration of 400 μg anti-OPN (SLAYGLR) neutralizing antibody or control IgG. Four laser spots were prepared in each eye. At day 14, the size of the CNV was evaluated by high-resolution angiography with fluorescein isothiocyanate (FITC)-dextran. Six wild-type or six knockout mice also received photocoagulation and processed for histology. mRNA expression of OPN, VEGF, and F4/80 macrophage antigen in laser-irradiated choroidal tissues was analyzed at day 3 in wild-type or knockout mice as well as in wild-type mice treated with anti-OPN antibody or control antibody.
Results:
Photocoagulation upregulated OPN expression in choroidal tissue. Histology did not uncover the effects of the lack of OPN on the healing of laser injury in choroid. The lack of OPN or systemic administration of anti-OPN antibody suppressed mRNA expression of VEGF and macrophage invasion in choroidal tissue. FITC-dextran angiography showed that lacking OPN or systemic anti-OPN antibody reduced the size of laser-induced CNV.
Conclusions:
OPN is upregulated in laser-irradiated choroidal tissue. Endogenous OPN is required for macrophage inflammation and VEGF expression in choroidal tissue and for CNV development after retinal photocoagulation in mice.
Insights
Osteopontin (OPN) is upregulated after laser injury and is essential for choroidal neovascularization (CNV) development. Lack of OPN or anti-OPN antibodies reduce inflammation and vascular endothelial growth factor (VEGF) expression, thereby inhibiting CNV.
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Background:
- Osteopontin (OPN) is a cytokine implicated in inflammation and tissue remodeling.
- Choroidal neovascularization (CNV) is a major cause of vision loss, driven by inflammatory processes.
- Vascular endothelial growth factor (VEGF) plays a critical role in the pathogenesis of CNV.
Purpose of the Study:
- To investigate the role of OPN in the development of CNV following retinal photocoagulation.
- To assess the impact of OPN deficiency and anti-OPN antibody administration on inflammation and VEGF expression in the choroid.
Main Methods:
- CNV was induced by laser photocoagulation in OPN-deficient and wild-type mice.
- Systemic administration of anti-OPN neutralizing antibody or control IgG was performed in wild-type mice.
- CNV size was quantified using fluorescein angiography, and mRNA expression of OPN, VEGF, and macrophage markers was analyzed.
Main Results:
- Photocoagulation led to increased OPN expression in choroidal tissue.
- OPN deficiency or anti-OPN antibody treatment suppressed VEGF mRNA expression and macrophage infiltration.
- Reduced CNV size was observed in OPN-deficient mice and those treated with anti-OPN antibodies.
Conclusions:
- Endogenous OPN is upregulated in response to laser-induced choroidal injury.
- OPN is crucial for mediating macrophage-driven inflammation and VEGF expression in the choroid.
- Targeting OPN may represent a therapeutic strategy for inhibiting CNV development.
