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Updated: Mar 13, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Tissue Plasminogen Activator as an Antiangiogenic Agent in Experimental Laser-Induced Choroidal Neovascularization in
Daisuke Ozone1, Takeshi Mizutani1, Miho Nozaki1
1Department of Ophthalmology and Visual Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Purpose:
We investigate the antiangiogenic efficacy of tissue plasminogen activator (tPA) on experimental laser-induced choroidal neovascularization (CNV) in mice.
Methods:
After CNV was induced by laser photocoagulation in 92 C57BL/6J wild-type mice, tPA (4 or 40 international units [IU]/μl) or PBS was injected intravitreally immediately after laser injury. Fluorescein angiography was performed on day 7 to grade CNV leakage. The CNV volume was measured by confocal microscopy in eyes enucleated 7 days after laser injury. Immunohistochemical studies were performed 3 days after laser injury to evaluate fibrin/fibrinogen and CD31 expression. The possible adverse effects of tPA were assessed by electroretinography (ERG) and histology on day 7.
Results:
Intravitreal administration of tPA significantly suppressed CNV leakage and CNV volume in a dose-dependent manner (P < 0.01). Intravitreal injection of tPA suppressed fibrin/fibrinogen and CD31 expression in laser-induced lesions. Histologic examination and ERG showed no evidence of retinal toxicity in eyes injected with tPA.
Conclusions:
Intravitreal injection of tPA suppressed fibrin/fibrinogen expression and laser-induced CNV. The current results suggested that tPA may be a potential therapeutic adjuvant for treating CNV.
Insights
Tissue plasminogen activator (tPA) effectively reduced choroidal neovascularization (CNV) leakage and volume in mice. This study suggests tPA as a potential therapeutic option for treating CNV.
Area of Science:
- Ophthalmology
- Angiogenesis Research
- Vascular Biology
Background:
- Choroidal neovascularization (CNV) is a leading cause of vision loss.
- Current treatments for CNV have limitations.
- Novel therapeutic strategies are needed to combat CNV progression.
Purpose of the Study:
- To evaluate the antiangiogenic effect of tissue plasminogen activator (tPA) on experimental laser-induced CNV in a mouse model.
- To determine the efficacy of intravitreal tPA in reducing CNV leakage and volume.
- To assess the impact of tPA on fibrin/fibrinogen and CD31 expression in CNV lesions.
Main Methods:
- CNV was induced by laser photocoagulation in C57BL/6J wild-type mice.
- Intravitreal injections of tPA (4 or 40 IU/μl) or PBS were administered immediately after laser injury.
- CNV leakage was assessed by fluorescein angiography, and CNV volume was measured by confocal microscopy.
- Immunohistochemistry, electroretinography (ERG), and histology were used to evaluate fibrin/fibrinogen, CD31 expression, and retinal toxicity.
Main Results:
- Intravitreal tPA significantly suppressed CNV leakage and volume in a dose-dependent manner (P < 0.01).
- tPA administration reduced fibrin/fibrinogen and CD31 expression in laser-induced CNV lesions.
- No retinal toxicity was observed with tPA treatment, as confirmed by ERG and histology.
Conclusions:
- Intravitreal injection of tPA effectively suppresses laser-induced CNV and associated biomarkers.
- tPA demonstrates antiangiogenic properties relevant to CNV treatment.
- tPA may serve as a promising therapeutic adjuvant for managing choroidal neovascularization.
