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Corneal and conjunctival epithelial cell surface proteins, primarily represented by membrane-associated mucins such as MUC1, MUC4, and MUC16, constitute the glycocalyx that protects the ocular surface. These heavily glycosylated proteins are essential for maintaining the stability of the tear film by providing a hydrophilic interface that allows tears to spread evenly across the eye and prevents desiccation. In ocular surface disorders like Dry Eye Disease (DED), the expression and glycosylation of these proteins are often reduced, leading to tear film instability, increased friction, and epithelial damage. Therapeutic agents like Rebamipide target these proteins by stimulating their expression and secretion, thereby restoring the ocular surface barrier and improving lubrication. Other treatments, such as Diquafosol, indirectly support these surface proteins by promoting the secretion of mucins and aqueous components from the epithelium and goblet cells via P2Y2 receptor activation.
Rebamipide increases the expression and secretion of membrane-associated mucins (MUC1, MUC4, MUC16) on the corneal and conjunctival surfaces to stabilize the tear film.
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