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<p>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 <i>ISLR</i> 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.</p>

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Possible involvement of the mesenchymal cell marker Meflin in regeneration after retinal injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月24日

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  • Daishi Okuda,
  • Shinji Mii,
  • Yuki Miyai,
  • Katsuhiro Kato,
  • Ryota Ando,
  • Yukihiro Shiraki,
  • Nobutoshi Esaki,
  • Kazuhisa Yamada,
  • Hideyuki Shimizu,
  • Hiroaki Ushida,
  • Hiroki Kaneko,
  • Koji M. Nishiguchi,
  • Atsushi Enomoto

摘要

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.