Interleukin-22 Ameliorates Dextran Sulfate Sodium-Induced Colitis through the Upregulation of lncRNA-UCL to Accelerate Claudin-1 Expression via Sequestering miR-568 in Mice

Figure 7

Elevation of lncRNA-UCL sequestered by miR-568 enhanced claudin-1 expression to maintain intestinal epithelial integrity induced by IL-22. (a) qRT-PCR was performed to determine the change in the expression of lncRNA-UCL and proinflammatory cytokines (TNF-α, IL-6, and IL-1β) at gene level after the knockdown of lncRNA-UCL and after IL-22 treatment in MODE-K cells. (b) In MODE-K cells, after the silencing of lncRNA-UCL expression and IL-22 treatment, changes in the expression of claudin-1, ZO-1, E-cadherin, and phosphorylated STAT3 protein were shown using western blotting analysis (c) while EDU assay was used to measure proliferation. (d) In MODE-K cells transfected with miR-568 mimics and treated with IL-22, western blot analysis was used to demonstrate changes in claudin-1, ZO-1, E-cadherin and phosphorylated STAT3 protein expression. (e) EDU assay was used to measure levels of proliferation. (f) In MODE-K cells, knockdown of lncRNA-UCL or interfering of miR-568 or simultaneously silencing both of lncRNA-UCL and miR-568, western blot analysis was used to show expression level changes of claudin-1, ZO-1, E-cadherin, and phosphorylated STAT3 protein. (g) EDU assay was used to measure proliferation. Data are presented as . ^###; ^##; ^# using Student’s -test.

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