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An-Katrien De Roo, Beatrijs Foets, Joost J van den Oord; Superficial Conjunctival Epithelium as the Main Producer of Protective Tear Component Cystatin SN. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1846.
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© ARVO (1962-2015); The Authors (2016-present)
CST1 is a gene known to be expressed in lacrimal glands. Its corresponding protein cystatin SN, is a component of human tear fluid, that is thought to play a protective role by inhibiting cysteine proteases. We investigated whether the conjunctival and corneal epithelia contribute to the production of cystatin SN and whether this production increases in response to injury.
From our Pathology files we selected formalin-fixed, paraffin-embedded tissues from 13 corneas from enucleated uveal melanomas, 5 donor corneal rims, 9 corneas with acute keratitis, 2 pterygia, 1 conjunctival naevocellular naevus, 1 conjunctival intraepithelial neoplasia, 1 conjunctival squamous cell carcinoma, and 3 lacrimal glands. Permissions from the local Ethics Committee and Biobank were obtained. Tissue sections were manually stained for cystatin SN.
All normal corneas showed strong and diffuse immunoreactivity for cystatin SN in the superficial layers of the conjunctival epithelium and corneal limbus, with an abrupt loss of staining in the more central corneal epithelium. Scarce immunoreactivity was observed in a proportion of epithelial cells lining the main excretory ducts and in a minority of secretory cells of the lacrimal glands. Gain of immunoreactivity occurred in the central corneal epithelium of injured corneas. The basal layer of conjunctival and corneal epithelium did not stain. Intraepithelial conjunctival neoplasia showed hyperplasia of the basal cell layers, lacking immunoreactivity. A minority of tumor cells within the nests of squamous cell carcinoma were stained. No reactivity was seen in naevus cells.
In contrast to current belief, these findings show that the conjunctiva, and not the lacrimal gland, is the main producer of cystatin SN in the anterior eye. Furthermore, the gain of corneal epithelial immunoreactivity in injured corneas supports the presumed role of CST1 in protecting the anterior ocular surface. The absence of staining in basal epithelial cells suggests that production of cystatin SN requires a certain level of cell maturation. And finally, cystatin SN can be proposed as a new and robust marker to distinguish between peripheral and central corneal epithelium in the normal cornea. Polymerase chain reaction will be conducted to confirm that this immunoreactivity is due to CST1 expression and not to uptake of the protein from the surrounding tear fluid.
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