Díaz Nicolás M, Sun Xizhang, Van Gelder Russell N, Lang Richard A, Buhr Ethan D
Department of Ophthalmology, University of Washington School of Medicine, Seattle, WA, USA.
Department of Ophthalmology, University of Washington School of Medicine, Seattle, WA, USA; Department of Neurobiology & Biophysics and Laboratory Medicine & Pathology, University of Washington School of Medicine, Seattle, WA, USA; Roger and Angie Karalis Johnson Retina Center, University of Washington School of Medicine, Seattle, WA, USA.
Cell Rep. 2025 Aug 26;44(8):116045. doi: 10.1016/j.celrep.2025.116045. Epub 2025 Jul 22.
The cornea is the transparent tissue at the ocular surface that generates most of the refractive power of the eye. Due to its exposed location, the cornea is uniquely in danger of injury. Rapid and efficient healing is required for high-acuity vision. Here, we show that epithelial corneal wounding induces Opn5, an opsin G-protein-coupled receptor (GPCR) sensitive to ultraviolet/violet light, at the cornea's surface in both mice and primates. The expression of corneal Opn5 is coincident with the direct light sensitivity of multiple pathways, including circadian rhythms, damage-response genes, and immune modulators. The presence of a violet-light:dark cycle substantially accelerates epithelial wound closure both in vivo and ex vivo. Corneas lacking Opn5 have markedly impaired wound healing. Violet light also accelerates wound healing in non-human primate corneas and induces gene expression similar to mice. These results demonstrate that corneal wounding induces direct photosensitivity via Opn5, which accelerates wound healing in the cornea.
角膜是眼表的透明组织，它产生眼睛的大部分屈光力。由于其暴露的位置，角膜特别容易受到损伤。为了实现高敏锐度视力，需要快速且高效的愈合。在此，我们表明，在小鼠和灵长类动物中，角膜上皮损伤均会在角膜表面诱导视蛋白5（Opn5）表达，视蛋白5是一种对紫外线/紫光敏感的视蛋白G蛋白偶联受体（GPCR）。角膜视蛋白5的表达与包括昼夜节律、损伤反应基因和免疫调节因子在内的多种途径的直接光敏感性一致。紫光：暗周期的存在在体内和体外均能显著加速上皮伤口闭合。缺乏视蛋白5的角膜伤口愈合明显受损。紫光还能加速非人类灵长类动物角膜的伤口愈合，并诱导与小鼠相似的基因表达。这些结果表明，角膜损伤通过视蛋白5诱导直接光敏感性，从而加速角膜伤口愈合。
