miR-200b is involved in intestinal fibrosis of Crohn’s disease

Chen, Yingwei; Ge, Wensong; Xu, Leiming; Qu, Chun-Ying; Zhu, Mingjie; Zhang, Wenzhu; Xiao, Yongtao

doi:10.3892/ijmm.2012.894

Cited by 83 publications

(47 citation statements)

References 41 publications

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“…The study indicated that significant changes in miRNA expression are associated with the late-stage disease process. The miR-200 family has been shown to downregulate ZEB1/Zeb2 proteins, which are involved in fibrotic gene expression (47). Our data showed downregulation of miR-200b, miR-200b-5p, and 200b-3p miR-200a-3p, indicating higher expression of Zeb1/Zeb2 and increased fibrosis, in agreement with the previous report of Igietseme et al (44).…”

Section: Discussionsupporting

confidence: 92%

MicroRNAs Modulate Pathogenesis Resulting from Chlamydial Infection in Mice

et al. 2017

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Not all women infected with chlamydiae develop upper genital tract disease, but the reason(s) for this remains undefined. Host genetics and hormonal changes associated with the menstrual cycle are possible explanations for variable infection outcomes. It is also possible that disease severity depends on the virulence of the chlamydial inoculum. It is likely that the inoculum contains multiple genetic variants, differing in virulence. If the virulent variants dominate, then the individual is more likely to develop severe disease. Based on our previous studies, we hypothesized that the relative degree of virulence of a chlamydial population dictates the microRNA (miRNA) expression profile of the host, which, in turn, through regulation of the host inflammatory response, determines disease severity. Thus, we infected C57BL/6 mice with two populations of Chlamydia muridarum, each comprised of multiple genetic variants and differing in virulence: an attenuated strain (Nigg A ) and a virulent strain (Nigg V ). Nigg A and Nigg V elicited upper tract pathology in 54% and 91% of mice, respectively. miRNA expression analysis in Nigg V -infected mice showed significant downregulation of miRNAs involved in dampening fibrosis (miR-200b, miR-200b-5p, and 200b-3p miR-200a-3p) and in transcriptional regulation of cytokine responses (miR-148a-3p, miR-152-3p, miR-132, and miR-212) and upregulation of profibrotic miRNAs (miR-142, and miR-147). Downregulated miRNAs were associated with increased expression of interleukin 8 (IL-8), CXCL2, IL-1␤, tumor necrosis factor alpha (TNF-␣), and IL-6. Infection with Nigg V but not Nigg A led to decreased expression of Dicer and Ago 2, suggesting that Nigg V interaction with host cells inhibits expression of the miRNA biogenesis machinery, leading to increased cytokine expression and pathology.

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Section: Discussionsupporting

confidence: 92%

MicroRNAs Modulate Pathogenesis Resulting from Chlamydial Infection in Mice

et al. 2017

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“…Intestinal fibrosis is a common serious complication of CD. In another study, they demonstrated that miR-200b could partially protect intestinal epithelial cells from fibrogenesis by suppressing EMT in vitro [60] . In summary, miR-200b played a potential role in maintaining intact of intestinal epithelium through inhibiting EMT and improving pathophysiology and clinical outcomes of IBD.…”

Section: Mirnas Regulate Intestinal Epithelial Barrier Functionmentioning

confidence: 98%

Implication of miRNAs for inflammatory bowel disease treatment: Systematic review

Chen¹,

Ren²,

Shi³

2014

WJGP

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Inflammatory bowel disease (IBD) is believed to develop via a complex interaction between genetic, environmental factors and the mucosal immune system. Crohn's disease and ulcerative colitis are two major clinical forms of IBD. MicroRNAs (miRNAs) are a class of small, endogenous, noncoding RNA molecules, and evolutionary conserved in animals and plants. It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation. MiRNAs are important in many biological processes, such as signal transduction, cellular proliferation, differentiation and apoptosis. Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease, especially IBD. Recent studies have identified altered miRNA profiles in ulcerative colitis, Crohn's disease and inflammatory bowel diseaseassociated colorectal cancer. In addition, emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD. MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway (e.g. , miR-146a, miR-146b, miR-122, miR-132, miR-126), intestinal epithelial barrier function (e.g. , miR-21, miR-150, miR-200b) and the autophagic activity (e.g. , miR-30c, miR-130a, miR-106b, miR-93, miR-196). This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis, their role as disease biomarkers, and perspective for future investigation and clinical application. Key words: Crohn's disease; Inflammatory bowel disease; MicroRNA; Treatment; Ulcerative colitis; Biomarker Core tip: MicroRNAs (miRNAs) are a class of small, noncoding RNA molecules that post-transcriptionally regulate gene and protein expression. Recent studies have identified altered miRNA profiles in inflammatory bowel disease (IBD). Special miRNAs which suppress functional targets have been found to play a critical role in regulating key pathogenic mechanism in IBD. In this review, we discuss the possibility to use miRNAs as biomarkers and therapeutic target in IBD.Chen WX, Ren LH, Shi RH. Implication of miRNAs for inflammatory bowel disease treatment: Systematic review. World

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“…[15][16][17][18] Targeted analysis of isolated miRNA families has also shown the difference between nonstricturing CD (NSCD) and SCD patients. 12,19 Here, we perform the first comprehensive miRNA profiling of CD serum samples to distinguish between different CD phenotypes. We identify miRNAs in serum associated with SCD and validate the results in independent cohorts of CD patients.…”

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confidence: 99%