MicroRNA‐132 and microRNA‐223 control positive feedback circuit by regulating FOXO3a in inflammatory bowel disease

Kim, Hye-Youn; Kwon, Hyeok Yi; Thi, Huyen Trang Ha; Lee, Ho Jae; Kim, Gwang Il; Hahm, Ki-Baek; Hong, Seok Pyo

doi:10.1111/jgh.13321

Cited by 49 publications

(38 citation statements)

References 35 publications

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“…It has been reported that miRNAs exert vital roles in a variety of inflammatory diseases, such as acute kidney injury [6], adipose tissue inflammation [7], inflammatory bowel disease [8], periapical lesions and human periodontal ligament fibroblast inflammation [9] and allergy and asthma [10]. In addition, a few studies have focused on the relationship between miRNAs and AP.…”

Section: Introductionmentioning

confidence: 99%

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Liu¹,

Zou²,

Wang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Acute pancreatitis contributes to high mortality in pancreatitis patients, and miRNAs play a vital role in the development of acute pancreatitis (AP), however, its precise biological role remains largely elusive. Methods: To clarify the potential mechanisms of miRNAs in AP, we built mouse models of mild acute pancreatitis (MAP) and moderate/ severe acute pancreatitis (SAP). MiRNA microarray analysis and Real-time quantitative PCR (qRT-PCR) were used to analyze the expression of miRNA in MAP/SAP. TargetScan software, dual-luciferase gene reporter assays and Western blotting were used to assess the target genes of miR-155-5p in AP. Results: miR-155-5p was significantly decreased in MAP/SAP mice compared to controls. In pancreatic acinar AR42J cells transfected with miR-155-5p mimic, the expression of Rela and Traf3 notably decreased in both the caerulein- and TLC-S-induced groups compared with the negative control (NC); however, the expression of Rela and Traf3 notably increased after transfection with miR-155-5p inhibitor. Combined analysis using the TargetScan software and dual-luciferase gene reporter assays indicated that Rela and Traf3 were both targeted by miR-155-5p. Meanwhile, the expression of Ptgs2 also decreased after transfection of the AR42J cells with miR-155-5p mimic. The opposite results were found when miR-155-5p inhibitor was transfected into the AR42J cells. In addition, we treated caerulein- and TLC-S-induced AR42J cells with the Rela inhibitor helenalin and found that the expression of Rela, Traf3 and Ptgs2 decreased compared with the NC, while the expression of miR-155-5p did not show any significant difference. Furthermore, we found that miR-155-5p was significantly down-regulated in pancreatitis patients. Conclusion: miR-155-5p inversely regulated AP development through the Rela/Traf3/Ptgs2 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Liu¹,

Zou²,

Wang³

et al. 2018

Cell Physiol Biochem

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“…MicroRNAs not only affect the cells that express them, but also enter other cells and modify their function. MicroRNA‐223 down‐regulates the inhibitor of kappa B by targeting forkhead box O3 , leading to activation of the proinflammatory nuclear factor kappa‐light‐chain‐enhancer of activated B cells signaling pathway. In addition, microRNA‐101 that binds to mitogen‐activated protein kinase phospatase1 mRNA 3′‐UTR and microRNA‐206 can stimulate production of proinflammation cytokines .…”

Section: Micrornas Dysregulated By Il‐4 In Primary Human Keratinocytesmentioning

confidence: 99%

IL‐4 dysregulates microRNAs involved in inflammation, angiogenesis and apoptosis in epidermal keratinocytes

Bao

Chau

Bao

et al. 2018

Microbiology and Immunology

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IL-4 plays an important role in the pathogenesis of atopic dermatitis (AD) by dysregulating many key factors at the transcriptional level. In this study, a microRNA array technique and IL-4 transgenic mice were used to demonstrate that IL-4 dysregulates microRNAs involved in inflammation, angiogenesis, lymphangiogenesis and apoptosis. Of the 372 common microRNAs examined, 26 and one microRNAs were found to be up-and down-regulated, respectively. MicroRNA-101-5p, À122-5p, À142-3p, À204-5p, À335-3p, À376a-3p, À378a-5p, À639 and À9-5p are among the most significantly up-regulated microRNAs. MicroRN A-147a, the only one that was down-regulated in the present study, attenuates TLR-induced inflammatory responses. These dysregulated microRNAs may provide post-transcriptional regulation of key genes in AD.

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“…By contrast, miR-31 expression increased while miR-21 , miR-155 and miR-146a levels decreased in colonic CD3 + T cells in UC remission [18]. Table 1 presents microRNAs with validated target transcripts in gut mucosa or cells of the immune system in the context of IBD or in different mouse models [16,19,20 • ,21 •• ,22–32]. …”

Section: Micrornas In Ibdmentioning

confidence: 99%

“…Abnormal expression of genes encoding barrier proteins has been linked to the development of IBD, CD, UC and other inflammatory-related diseases [5,7,34]. Several microRNAs, whose expression changed in IBD [16,19,20 • ,21 •• ,22–32,36] have been shown to target transcripts encoding some of the above proteins in the context of gut inflammatory diseases. For example, by targeting Claudin 8 , pro-inflammatory miR-223 was instrumental in allowing IL23 pathway to initiate trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice [32].…”

Section: Micrornas In Ibmentioning

confidence: 99%

MicroRNAs in intestinal barrier function, inflammatory bowel disease and related cancers — their effects and therapeutic potentials

Tili

Michaille

Piurowski

et al. 2017

Current Opinion in Pharmacology

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The initiation and development or inflammatory bowel disease (IBD) and associated colorectal cancers, have been linked to inflammation. MicroRNAs are non-coding regulators of gene expression that have gained great attention due to their capability to regulate the expression of a number of target transcripts. It is now generally admitted that microRNAs are instrumental in gut pathologies, in particular through their targeting of transcripts encoding proteins of the intestinal barrier (IB) and their regulators. Intense research is conducted to identify microRNAs susceptible to be used as biomarkers and to design new therapeutic approaches based upon using synthetic microRNA mimics and inhibitors as well as finding new drugs capable to restore or modify microRNA expression in the context of gut pathologies.

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MicroRNA‐132 and microRNA‐223 control positive feedback circuit by regulating FOXO3a in inflammatory bowel disease

Abstract: Our findings provided the evidences that miR-132 and 223 are critical mediators in positive circuit for pathogenesis of IBD by negatively regulating FOXO3a to enhance the expression of inflammatory cytokines and can be a good therapeutic target for IBD treatment.

Cited by 49 publications

References 35 publications

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

IL‐4 dysregulates microRNAs involved in inflammation, angiogenesis and apoptosis in epidermal keratinocytes

MicroRNAs in intestinal barrier function, inflammatory bowel disease and related cancers — their effects and therapeutic potentials

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