# Photoreceptor induction in wounded corneas

> **NIH NIH R01** · UNIVERSITY OF WASHINGTON · 2024 · $441,250

## Abstract

Project Summary/Abstract
The cornea is the optically clear, curved tissue that provides the majority of refractive power in
the eye. Improper healing of corneal wounds is a serious issue that can lead to blindness or
permanent refractive visual complications. We have demonstrated that the cornea becomes
intrinsically photoreceptive after injury, and it is able to entrain its circadian clock to light cycles
in vitro. We have observed that the rate healing of wounded mouse corneas is accelerated by
violet light both in vivo and ex vivo. We have identified a class of highly motile Opn5-expressing
epithelial cells induced in the cornea after wounding. Opn5 is an opsin protein which is sensitive
to short wavelength light. Mice which lack Opn5 show aberrant responses to corneal wounding,
such as impaired re-epithelialization and stromal abnormalities. The central hypothesis of this
proposal is that light modulates corneal wound healing via an Opn5-dependent mechanism. We
have also found evidence of non-photic effects mediated by Opn5. The specific aims of this
project include the following: (Aim 1) testing the light regimen necessary for photic healing
acceleration in murine corneas, (Aim 2) characterizing the mechanism of signal transduction
within Opn5-expressing cells, and (Aim 3) testing the hypothesis that diffusible factors function
in the induction of Opn5 expression and its communication with the rest of the cornea. Our
approach will be to utilize both in vivo and ex vivo experimentation with a number of mouse
models in which the Opn5 cells can be visualized or have their molecular constituents isolated
from whole corneal cell lysate. We will also use cultured cell lines to uncover the factor or
factors necessary to induce Opn5. The innovation of this project lies in applying recently
discovered extra-retinal photoreception to analyses of wound healing and the health of the
corneal surface. Another aspect of this innovation will be to extend the results of mouse studies
to corneal cells from human and non-human primates to analyze the translational potential of
the observations made in mouse models. The potential impact of this work will be to harness the
role light plays in corneal wound healing through opsin agonists/ antagonists to facilitate wound
closure and the avoidance of scarring.

## Key facts

- **NIH application ID:** 10976990
- **Project number:** 1R01EY035319-01A1
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Ethan D Buhr
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $441,250
- **Award type:** 1
- **Project period:** 2024-09-01 → 2029-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10976990

## Citation

> US National Institutes of Health, RePORTER application 10976990, Photoreceptor induction in wounded corneas (1R01EY035319-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10976990. Licensed CC0.

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