Role of miR-19a targeting TNF-α in mediating ulcerative colitis

Objective. Ulcerative colitis (UC) is a widely studied inflammatory disease associated with differential expression of genes involved in immune function, wound healing, and tissue remodeling. MicroRNAs have been reported to play a role in various cancer types. However, the mechanism of how microRNAs regulate UC remains unclear. Methods. In the present study, we investigated the role of miR-19a and tumor necrosis factor (TNF)-alpha in human colon tissues with UC and dextran sodium sulfate (DSS)-induced experimental colitis. Results. We identified that the expression of miR-19a was significantly reduced and TNF-alpha was remarkably increased in human colon tissue with UC. Moreover, this observation of miR-19a and TNF-alpha was also occurred in DSS-treated mice colitis. Further, we observed that miR-19a directly regulated TNF-alpha expression because miR-19a can suppress the expression of wild-type TNF-alpha reporter, but not the mutant form. The expression of inflammatory factors TNF-alpha, IL-8, and GM-GSF were significantly elevated upon application of miR-19a inhibitor. Conclusion. Taken together, this study determines the levels of miR-19a and TNF-alpha in both DSS-induced experimental murine colitis and human UC and further demonstrates that miR-19a might directly regulate TNF-alpha. The findings may provide a new insight in the clinical treatment of UC.