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Updated: May 10, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Role of miR-19a targeting TNF-α in mediating ulcerative colitis
Bin Chen1, Shifeng She, Detang Li
1Department of Gastroenterology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
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)-α 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-α was remarkably increased in human colon tissue with UC. Moreover, this observation of miR-19a and TNF-α was also occurred in DSS-treated mice colitis. Further, we observed that miR-19a directly regulated TNF-α expression because miR-19a can suppress the expression of wild-type TNF-α reporter, but not the mutant form. The expression of inflammatory factors TNF-α, 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-α in both DSS-induced experimental murine colitis and human UC and further demonstrates that miR-19a might directly regulate TNF-α. The findings may provide a new insight in the clinical treatment of UC.
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