Decoding the molecular complexity governing corneal wound closure in vivo

The cornea is the transparent tissue on the anterior surface of the eye. It is notably composed of a squamous stratified epithelium that forms a barrier protecting the ocular chamber. As the cornea is avascular, the delivery of nutrients and growth factors, required for corneal physiology, is essential. These nutrients and factors come from 1) the epithelium itself, 2) the innervation, and 3) the tear film, which together form the corneal microenvironment. Disturbances of this microenvironment, in the context of injury, aging or corneal pathology, can lead to progressive corneal opacification, resulting in blindness. More than 28 million people suffer from mono- or bilateral corneal blindness, making it the fourth cause of blindness worldwide. Corneal abrasion is the most common eye injury encountered in clinics, but poorly studied, making it a major issue in ophthalmology. It is characterized by a transient rupture in the integrity and cellular cohesion of the epithelial barrier, which are brought back thanks to a corneal wound healing process. The aim of this study is therefore to highlight the molecular impact of corneal abrasion on the microenvironment, and more specifically on the tear film. We performed a longitudinal study to identify a specific proteome of tears before and after corneal abrasion in mice. The corneal abrasion was performed unilaterally on female mice. Tear fluid samples were collected from the wounded eye and the contralateral eye before corneal abrasion and during the wound healing process up to 24hrs post-abrasion.