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Updated: Jun 26, 2026
Müller Glia Cell Activation in a Laser-induced Retinal Degeneration and Regeneration Model in Zebrafish
Published on: October 27, 2017
Possible involvement of the mesenchymal cell marker Meflin in regeneration after retinal injury
Daishi Okuda1,2, Shinji Mii3,4,5, Yuki Miyai1
1Department of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Abstract:
Pathological tissue remodeling, including choroidal neovascularization (CNV) and fibrosis, is central to the development of retinal diseases such as age-related macular degeneration; however, its molecular mechanisms remain incompletely defined. We examined the intraocular expression patterns of Meflin encoded by the ISLR gene, a mesenchymal stromal cell marker with anti-fibrotic properties, in human surgical specimens and mouse retinal tissues, and evaluated its involvement in a retinal injury mouse model. Meflin expression was detected in fibroblast-like stromal cells within human proliferative vitreoretinopathy / proliferative diabetic retinopathy fibrovascular membranes and the ciliary body, lens epithelium, retinal pigment epithelium, optic nerve meningeal cells, and choroidal perivascular fibroblast-like cells of the mouse eye. Lineage-tracing using a Meflin reporter mouse line revealed accumulation of Meflin-lineage cells within laser-induced CNV lesions. Notably, adeno-associated virus-mediated Meflin overexpression increased CNV volume in the acute phase of retinal injury but suppressed subretinal fibrosis after the CNV growth phase. These findings suggest that Meflin overexpression modulates angiogenic and fibrotic remodeling after retinal injury in a phase-dependent manner, consistent with reported roles in cancer and fibrotic diseases. These results improve understanding of retinal disease pathology and identify Meflin as a potential target for future therapeutic studies on proliferative and fibrotic retinal diseases.
Insights
Meflin, a stromal cell marker, influences both blood vessel growth (angiogenesis) and fibrosis in retinal injury models. Its overexpression promotes early vessel growth but later suppresses fibrosis, suggesting phase-dependent therapeutic potential.
Area of Science:
- Ophthalmology
- Molecular Biology
- Tissue Engineering
Background:
- Pathological tissue remodeling, including choroidal neovascularization (CNV) and fibrosis, drives retinal diseases like age-related macular degeneration.
- The precise molecular mechanisms underlying these remodeling processes are not fully understood.
Purpose of the Study:
- To investigate the intraocular expression patterns of Meflin (encoded by the ISLR gene), a mesenchymal stromal cell marker with anti-fibrotic properties.
- To evaluate Meflin's role in a mouse model of retinal injury, specifically laser-induced CNV.
Main Methods:
- Examined Meflin expression in human surgical specimens (proliferative vitreoretinopathy/proliferative diabetic retinopathy fibrovascular membranes) and mouse retinal tissues.
- Utilized a Meflin reporter mouse line for lineage tracing in laser-induced CNV lesions.
- Overexpressed Meflin using adeno-associated virus (AAV) in a mouse retinal injury model.
Main Results:
- Meflin was detected in various ocular cells, including fibroblast-like stromal cells in human membranes and mouse ocular tissues.
- Meflin-lineage cells accumulated in laser-induced CNV lesions.
- AAV-mediated Meflin overexpression transiently increased CNV volume but subsequently suppressed subretinal fibrosis.
Conclusions:
- Meflin overexpression modulates angiogenic and fibrotic remodeling in retinal injury in a phase-dependent manner.
- These findings enhance the understanding of retinal disease pathology.
- Meflin represents a potential therapeutic target for proliferative and fibrotic retinal diseases.
