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MiRNA-374b-5p and miRNA-106a-5p are related to inflammatory bowel disease via regulating IL-10 and STAT3 signaling pathways

BMC gastroenterology, 2022-11, Vol.22 (1), p.1-492, Article 492 [Peer Reviewed Journal]

COPYRIGHT 2022 BioMed Central Ltd. ;2022. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2022 ;ISSN: 1471-230X ;EISSN: 1471-230X ;DOI: 10.1186/s12876-022-02533-1 ;PMID: 36437465

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  • Title:
    MiRNA-374b-5p and miRNA-106a-5p are related to inflammatory bowel disease via regulating IL-10 and STAT3 signaling pathways
  • Author: Li, Dongjie ; Liu, Liyuan ; Du, Xiancai ; Ma, Wen ; Zhang, Jing ; Piao, Wenhua
  • Subjects: Antibodies ; Bioinformatics ; CD4 antigen ; CD4+ T cells ; Cell differentiation ; Chromosome 5 ; Crohn's disease ; Cytokines ; Development and progression ; Etiology ; Flow cytometry ; Gastroenterology ; Gastrointestinal diseases ; Gene expression ; Genetic aspects ; Health aspects ; Helper cells ; IL-10 ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Interleukin 10 ; Intestine ; Janus kinase ; Lymphocytes ; Lymphocytes T ; MicroRNA ; MicroRNAs ; miRNA ; Pathogenesis ; Plasmids ; Proteins ; Reagents ; Remission (Medicine) ; Signal transduction ; STAT3 ; Stat3 protein ; Ulcerative colitis ; Western blotting ; γ-Interferon
  • Is Part Of: BMC gastroenterology, 2022-11, Vol.22 (1), p.1-492, Article 492
  • Description: Abstract Background Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is one of the most frequent gastrointestinal disorders worldwide. Although the actual etiology of IBD remains unclear, growing evidence suggests that CD4 + T cells-associated cytokines, including interferon (IFN)- γ , interleukin (IL)-10 and IL-17A, are crucial for the occurrence of IBD. It has been reported that there is a positive association between miRNAs and IBD development. In this study, we investigated the roles of hsa-miRNA-374b-5p(miRNA-374b-5p) and hsa-miRNA-106a-5p(miRNA-106a-5p) in regulating IBD development. Methods Serum was obtained from vein blood of IBD patients and healthy controls, qRT-PCR was performed to study the expression of miRNA-374b-5p and miRNA-106a-5p. Furthermore, we investigate the effects of overexpression or inhibition of miRNA-374b-5p on naïve CD4  +  T cell subsets differentiation from vein blood of healthy controls by RT-qPCR, flow cytometry and western blot. And more the prediction and confirmation of the targeting genes of miRNA-374b-5p and miRNA-106a-5p were performed by bioinformatics softwares and dual-luciferase reporter assay. Results The results showed that miRNA-106a-5p and miRNA-374b-5p were significantly overexpressed in IBD patients. MiRNA-374b-5p could enhance Th1/Th17 cell differentiation and was related to IBD pathogenesis. MiRNA-374b-5p overexpression induced the mRNA expression of IL-17A and IFN- γ , and suppressed that of IL-10 in T cells. MiRNA-374b-5p inhibition decreased the mRNA expression of IL-17A and IFN-γ, while upregulated that of IL-10 in T cells. These qPCR data were further verified at protein level by western blotting and flow cytometry. In addition, dual-luciferase reporter (DLR) assay indicated that miRNA-374b-5p was directly targeted by IL-10, a key anti-inflammatory cytokine for preventing the occurrence of IBD. Meanwhile, STAT3 was identified as a target gene of miRNA-106a-5p by DLR assays. Further analysis revealed that miRNA-374b-5p regulated JAK1 and STAT3 pathways in CD4 + T cells via IL-10/STAT3 axis. MiRNA-374b-5p overexpression remarkably decreased the mRNA expression and phosphorylated (ser-727) protein levels of STAT3, while miRNA-374b-5p inhibition had the opposite effects. Conclusion MiRNA-374b-5p and miRNA-106a-5p may contribute to IBD development by regulating IL-10/STAT3 signal transduction.
  • Publisher: London: BioMed Central Ltd
  • Language: English
  • Identifier: ISSN: 1471-230X
    EISSN: 1471-230X
    DOI: 10.1186/s12876-022-02533-1
    PMID: 36437465
  • Source: GFMER Free Medical Journals
    PubMed Central
    Springer Nature OA/Free Journals
    ROAD: Directory of Open Access Scholarly Resources
    ProQuest Central
    DOAJ Directory of Open Access Journals
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