Fig. 5

IL-17A facilitated repair of oxidative stress-induced barrier dysfunction. ARPE-19 cells were cultured in DMEM/F12 with 1% FBS for 7 days until they reached the appropriate cell confluence. A ARPE-19 cells were cotreated with 300 μM H₂O₂ and IL-17A (100 ng/ml) in the Transwell insert for 16 h, and immunofluorescence staining was performed with an anti-ZO-1-specific antibody in ARPE-19 monolayers in vitro. Scale bar = 75 μm. B To analyze the permeability function, ARPE-19 cells were cotreated with 300 μM H₂O₂ and IL-17A (100 ng/ml) in the Transwell insert for 16 h. FITC-dextran (100 μg/ml) was added after treatment, and the fluorescent content was measured at 485/538 nm excitation/emission wavelengths using a luminometer at 10-16 h. Statistical differences were determined by one-way ANOVA and Tukey’s multiple comparisons test. Data are presented as the mean ± SEM (****P < 0.0001). The data shown are representative of three independent experiments with similar results. C–G The mRNA expression of ZO-1, OCLN, CLDN-3, CLDN-10, and CLDN-19 in eyes isolated from WT and IL-17A^−/− mice (N = 6) at 28 days after laser injury was analyzed using RT‒qPCR with specific primers. Statistical differences were determined by two-way ANOVA and Sidak's multiple comparisons test. Data are presented as the mean ± SEM (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). The data shown are representative of three independent experiments with similar results