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Corneal and tear film mucins are high-molecular-weight, heavily glycosylated proteins that are essential for maintaining the stability and health of the ocular surface (Gipson, 2004). They are divided into two main classes: membrane-associated mucins (MUC1, MUC4, and MUC16), which form the glycocalyx on the corneal and conjunctival epithelium, and secreted mucins (primarily MUC5AC), which are produced by conjunctival goblet cells (Mantelli & Argüeso, 2008). These mucins provide lubrication, facilitate the spread of the tear film, and act as a protective barrier against pathogens and environmental stressors (Dartt, 2004). In diseases such as dry eye (keratoconjunctivitis sicca) and Sjögren's syndrome, mucin expression is often significantly reduced or altered, leading to tear film instability and epithelial damage (Argüeso et al., 2002). Therapeutic interventions include mucin secretagogues like diquafosol, which stimulates MUC5AC secretion via P2Y2 receptors, and rebamipide, which increases the expression of both membrane-associated and secreted mucins (Koh et al., 2013; Urashima et al., 2004). Additionally, anti-inflammatory treatments like cyclosporine and lifitegrast may indirectly support mucin production by reducing the inflammatory environment that suppresses goblet cell function (Pflugfelder et al., 2008).
Stimulation of mucin secretion from goblet cells and upregulation of membrane-associated mucin expression in corneal and conjunctival epithelial cells to restore tear film stability (Koh et al., 2013; Urashima et al., 2004).
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