Abstract
Instability of the tear film (TF) protecting the ocular surface results in dry eye syndrome (DES), the most prevalent public health ophthalmic disease affecting the quality of life of 10 to 30% of the human population worldwide. Although the impact of the tear film lipid layer (TFLL) and of the aqueous tears (AT) to the TF stability is extensively studied, in contrast the contribution of the secretory mucins (SM) and of the membrane-associated mucins (MAM), i.e., one of the most abundant molecular classes in AT and in the corneal epithelium respectively, remains poorly defined. However, it is well known that in DES both types of mucins are quantitatively or qualitatively deficient. Numerous studies since the 1990s until now have proposed direct involvement of SM and MAM in the material properties (viscoelasticity, hydration, and protection of the ocular surface; synergistic cooperation with the rest of the TF layers; etc.) and stability of TF. These theories will be reviewed here in the context of the classical and modern in vitro and in vivo results that allow their reappraisal and in view of the novel mucin secretion enhancing pharmaceuticals, which have opened innovative routes for the therapy of DES.
Highlights
Tear film (TF) is composite wetting film which consists of tear film lipid layer (TFLL) at the air/tear surface and underlying aqueous tear (AT) positioned over the glycocalyx of the corneal epithelium [1,2]
Important conclusion from the review of the interdisciplinary research accumulated up to now is that secretory mucins (SM) and membrane associated mucins (MAM), which span across the entire tear fluid, from the corneal surface to the air/tear surface [1,2], may ensure the synchronization between the different layers of the TF
Secretory mucins may facilitate the spreading of TFLL [2,37,40] and the mucoaqueous gel ensures surface chemistry protection of the MAM at the surface of the corneal epithelium cells [11,14,17,26,27,28,29]
Summary
Tear film (TF) is composite wetting film which consists of tear film lipid layer (TFLL) at the air/tear surface and underlying aqueous tear (AT) positioned over the glycocalyx of the corneal epithelium [1,2]. Tiffany concluded that the non-Newtonian behavior of whole human tears “cannot be explained by the amount of mucin present” and that “hetero-protein interactions, possibly electrostatic, involving lipid-binding-induced structural changes to tear lipocalin, significantly contribute to the viscosity of human tears” [16]. The reasons for such discrepancy between the hypothesized role of the gel-forming MUC5AC for the shear thinning-properties and the underlying structure of tears in open eye and the experimental findings of Tiffany might be due to couple of reasons.
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