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Updated: Dec 5, 2025
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
MicroRNAs in laser-induced choroidal neovascularization in mice and rats: their expression and potential therapeutic
Bridget Martinez1, Philip V Peplow2
1Physical Chemistry and Applied Spectroscopy, Chemistry Division, Los Alamos National Laboratory, Los Alamos, NM, USA; Department of Medicine, St. Georges University School of Medicine, Grenada.
Abstract:
Choroidal neovascularization characterizes wet age-related macular degeneration. Choroidal neovascularization formation involves a primarily angiogenic process that is combined with both inflammation and proteolysis. A primary cause of choroidal neovascularization pathogenesis is alterations in pro- and anti-angiogenic factors derived from the retinal pigment epithelium, with vascular endothelium growth factor being mainly responsible for both clinical and experimental choroidal neovascularization. MicroRNAs (miRNAs) which are short, non-coding, endogenous RNA molecules have a major role in regulating various pathological processes, including inflammation and angiogenesis. A review of recent studies with the mouse laser-induced choroidal neovascularization model has shown alterations in miRNA expression in choroidal neovascularization tissues and could be potential therapeutic targets for wet age-related macular degeneration. Upregulation of miR-505 (days 1 and 3 post-laser), miR-155 (day 14) occurred in retina; miR-342-5p (days 3 and 7), miR-126-3p (day 14) in choroid; miR-23a, miR-24, miR-27a (day 7) in retina/choroid; miR-505 (days 1 and 3) in retinal pigment epithelium/choroid; downregulation of miR-155 (days 1 and 3), miR-29a, miR-29b, miR-29c (day 5), miR-93 (day 14), miR-126 (day 14) occurred in retinal pigment epithelium/choroid. Therapies using miRNA mimics or inhibitors were found to decrease choroidal neovascularization lesions. Choroidal neovascularization development was reduced by overexpression of miR-155, miR-188-5p, miR-(5,B,7), miR-126-3p, miR-342-5p, miR-93, miR-126, miR-195a-3p, miR-24, miR-21, miR-31, miR-150, and miR-184, or suppression of miR-505, miR-126-3p, miR-155, and miR-23/27. Further studies are warranted to determine miRNA expression in mouse laser-induced choroidal neovascularization models in order to validate and extend the reported findings. Important experimental variables need to be standardized; these include the strain and age of animals, gender, number and position of laser burns to the eye, laser parameters to induce choroidal neovascularization lesions including wavelength, power, spot size, and duration.
Insights
MicroRNAs (miRNAs) show altered expression in wet age-related macular degeneration, offering potential therapeutic targets. Modulating specific miRNAs can reduce choroidal neovascularization, paving the way for new treatments.
Area of Science:
- Ophthalmology
- Molecular Biology
- Genetics
Background:
- Wet age-related macular degeneration (AMD) is characterized by choroidal neovascularization (CNV), driven by angiogenesis, inflammation, and proteolysis.
- Alterations in angiogenic factors, particularly vascular endothelium growth factor (VEGF), are key to CNV pathogenesis.
- MicroRNAs (miRNAs), short non-coding RNA molecules, regulate pathological processes like inflammation and angiogenesis.
Purpose of the Study:
- To review recent studies on miRNA expression in a mouse laser-induced CNV model.
- To identify potential therapeutic targets for wet AMD based on miRNA alterations.
- To evaluate the efficacy of miRNA-based therapies in reducing CNV lesions.
Main Methods:
- Analysis of miRNA expression profiles in retinal and choroidal tissues at various time points post-laser induction of CNV in mice.
- Review of studies investigating the effects of miRNA mimics or inhibitors on CNV development.
- Examination of CNV lesion size following modulation of specific miRNA expression levels.
Main Results:
- Significant alterations in the expression of various miRNAs (e.g., miR-505, miR-155, miR-342-5p, miR-126-3p, miR-23a, miR-24, miR-27a, miR-29a/b/c, miR-93) were observed in CNV tissues.
- Therapeutic interventions using miRNA mimics or inhibitors demonstrated a reduction in CNV lesion size.
- Overexpression of certain miRNAs (e.g., miR-155, miR-126-3p) or suppression of others (e.g., miR-505) effectively reduced CNV development.
Conclusions:
- miRNA expression is significantly altered in the context of CNV, highlighting their role in wet AMD pathogenesis.
- miRNAs represent promising therapeutic targets for wet AMD, with interventions showing potential to reduce CNV.
- Further standardization of experimental models is crucial for validating and advancing miRNA-based therapies for wet AMD.
