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Yuichi Hori, Yuzo Deguchi, Junya Ashizawa, Koichiro Hitani, Tomoaki Shiba, Yoshitsugu Saishin, Takatoshi Maeno; Evaluation of MUC16 Expression Induced by Benzalkonium Chloride on the Ocular Surface Epithelium. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1956.
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© ARVO (1962-2015); The Authors (2016-present)
To evaluate the effect of the expression of membrane-associated mucin MUC 16 induced by benzalkonium chloride (BAC) in a human conjunctival epithelial (HCjE) cell line.
HCjE cells were grown to confluence in serum-free medium and switched to DMEM/F12 with 10% fetal bovine serum for 5 days to promote differentiation and express membrane-associated mucins. The cells then were exposed to 0.001%, 0.005%, and 0.01% BAC for 1 minute. BAC cytotoxicity on the HCjE cells was examined using a WST-1 assay. Quantitative real-time polymerase chain reaction (PCR) was performed to investigate the gene expression of MUC16 mRNA. To evaluate the mucin-associated ocular surface protection, a rose bengal uptake assay was performed.
The WST-1 assay showed that cell viability values after 1-minute exposure of 0.001%, 0.005%, and 0.01% BAC were 94.2%, 90.8%, and 86.2%, respectively, meaning that the cytotoxicity resulting from these exposures was mild. Nevertheless, MUC16 mRNA expression decreased significantly to 0.65, 0.43, and 0.33, respectively (p < 0.005, ANOVA). The rose bengal uptake assay showed that exclusion of the dye was reduced significantly in cells with all BAC concentrations (p < 0.005, ANOVA).
These results suggested that even short exposure to BAC down-regulates MUC16 expression and disrupts the disadhesive protective barrier for the ocular surface epithelial cells.
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