Objective: To investigate the effect of travoprost on changes of actin cytoskeletal and β-catenin protein in the cultured human trabecular meshwork (HTM) cells treated with dexamethasone (DEX).
Methods: It was a control experiment study. The HTM cells were cultured in vitro and divided into control group, DEX (1 × 10(-6) mol/L) group, travoprost (1 × 10(-6) mol/L) group, and DEX (1 × 10(-6) mol/L) plus travoprost (1 × 10(-6) mol/L) group. F-actin in the HTM cells was detected by FITC-phalloidin and observed under a fluorescence microscope. The expression of β-catenin was determined by immunofluorescence and western-blot. Statistical analysis was performed using SPSS13.0 software. The difference of β-catenin expression among groups was analyzed through variance analysis and, further by q test.
Results: The cultured HTM cells were identified by immunohistochemistry. A reorganization of actin cytoskeletal and a formation of cross linked actin networks (CLANs) were seen in the HTM cells treated with DEX, which were partially reversed by the treatment with DEX plus travoprost. An increase of the expression of β-catenin was discovered in the HTM cells treated with DEX, which was also partially reversed by the treatment with DEX plus travoprost. The amount of β-catenin protein in untreated control group, DEX group, DEX plus travoprost group and travoprost group were 0.84 ± 0.03, 1.65 ± 0.05, 1.21 ± 0.05, and 0.65 ± 0.04, respectively. Expression of β-catenin was significantly (F = 143.07, P < 0.05) different when compared untreated control group with DEX group (q = 15.32, P < 0.05), untreated control group with DEX plus travoprost group (q = 11.40, P < 0.05), DEX group with DEX plus travoprost group (q = 9.38, P < 0.05), DEX group with travoprost group (q = 16.55, P < 0.05), and DEX plus travoprost group with travoprost group (q = 14.31, P < 0.05). No difference was found in untreated control group and travoprost group (q = 2.84, P > 0.05).
Conclusions: Our results suggest that reversion of the changes of actin organization and β-catenin by travoparost in the HTM cells treated with DEX may partially elucidate the mechanism of action of increasing outflow by which travoprost reduces intraocular pressure.