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MicroRNA-155 is involved in the pathogenesis of ulcerative colitis by targeting FOXO3a
Min Min1, Lihua Peng, Yunsheng Yang
1*Department of Gastroenterology and Hepatology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing, China; and †Institute of Digestive Diseases, Chinese PLA General Hospital, Beijing, China.
Background:
MicroRNAs (miRNAs) are important posttranscriptional regulators of gene expression. The precise role of miRNAs in ulcerative colitis (UC) is not completely understood. The purpose of this study was to identify miRNAs that are induced in patients with active UC and to assess the effect of miR-155 on improving intestinal inflammation.
Methods:
The miRNA profiles in patients with active UC (n = 20) and healthy subjects (n = 16) were examined using miRNA microarrays. miR-155 upregulation was confirmed by quantitative RT-PCR. Regulation of the target gene FOXO3a expression by miR-155 was assessed using luciferase reporter construct assays and miR-155 mimic or inhibitor transfections. The effects of FOXO3a or miR-155 on IκBα or IL-8 were detected by Western blot or enzyme-linked immunosorbent assay in HT29 cells, respectively.
Results:
We identified 68 miRNAs that were differentially expressed (33 upregulated and 35 downregulated) in patients with active UC compared with healthy controls. One of the upregulated miRNAs in the UC tissue was miR-155 (1.22-fold, P < 0.03), which plays a key role in the regulation of inflammatory pathways. In patients with active UC, miR-155 was significantly upregulated, and the expression of FOXO3a dramatically decreased. Luciferase reporter assays demonstrated that miR-155 directly targets FOXO3a and affects the protein expression of FOXO3a in HT29 cells. Moreover, silenced FOXO3a and the overexpression of miR-155 increased the levels of IL-8 in TNF-α-treated HT29 cells by suppressing the inhibitory IκBα.
Conclusions:
miR-155 appears to play a role in the intestinal inflammation of patients with active UC by downregulating the expression of FOXO3a. This process may activate the nuclear factor kappa B signaling pathway.
Insights
MicroRNA-155 (miR-155) is upregulated in ulcerative colitis (UC) and drives intestinal inflammation by targeting FOXO3a, potentially activating NF-κB signaling. This finding offers new insights into UC pathogenesis.
Area of Science:
- Molecular Biology
- Genetics
- Immunology
Background:
- MicroRNAs (miRNAs) are key posttranscriptional gene regulators.
- The role of miRNAs in ulcerative colitis (UC) pathogenesis requires further elucidation.
- Identifying specific miRNAs in active UC can reveal novel therapeutic targets.
Purpose of the Study:
- To identify differentially expressed miRNAs in active UC patients.
- To investigate the role of miR-155 in intestinal inflammation.
- To assess the therapeutic potential of targeting miR-155 or its downstream effectors.
Main Methods:
- miRNA microarrays and quantitative RT-PCR for miRNA profiling.
- Luciferase reporter assays and transfections to study gene regulation.
- Western blot and ELISA to detect protein and cytokine levels.
Main Results:
- Identified 68 differentially expressed miRNAs in active UC patients.
- miR-155 was significantly upregulated in active UC and directly targets FOXO3a.
- miR-155 overexpression and FOXO3a silencing increased IL-8 via IκBα suppression.
Conclusions:
- miR-155 contributes to intestinal inflammation in active UC by downregulating FOXO3a.
- This downregulation may activate the nuclear factor kappa B (NF-κB) signaling pathway.
- miR-155 represents a potential therapeutic target for ulcerative colitis.
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