MicroRNA‐199b expression level and coliform count in irritable bowel syndrome

Mansour, M.; Sabbah, Norhan A.; Mansour, S.; Ibrahim, Abdallah

doi:10.1002/iub.1495

Cited by 11 publications

(12 citation statements)

References 42 publications

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“…The correlation between miRNAs and IBS has been concerned recently. The alternation of miRNAs were found in IBS, and study confirmed the role of miRNAs in IBS with increased gut permeability [ 19 – 23 ]. MiR-29a has been confirmed to take part in the regulation of intestinal membrane permeability in IBS.…”

Section: Discussionmentioning

confidence: 78%

“…Studies showed that miRNAs take part in a lot of pathophysiologic processes including inflammation, and its regulation of immune response plays an important role in the process of colony-stimulating factor and pathogen invasion [ 18 ]. In recent years, studies on correlation between miRNA and IBS have been concerned, which have shown that alterations of microRNAs (miRNAs) levels have affected IBS, and certificated the role of microRNAs in IBS with increased gut permeability [ 19 – 23 ].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats

et al. 2017

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BackgroundThe whole pathogenesis of diarrhea-predominant irritable bowel syndrome(IBS-D) is poorly understood. Our goal was to evaluate the expression change of microRNA-29a(miR-29a) in colonic epithelial cells in IBS rats and clarify the mechanism of miR-29a increasing the intestinal membrane permeability through aquaporins(AQPs).MethodsThe IBS-D rats models were induced by rectal distention pressure combining with extremities constraint. The colonic epithelial cells were divided into four groups. A: normal group. B: IBS-D control group. C: IBS-D +miR-29a NC. D: IBS-D + miR-29a antagomir. The expression of miR-29a, the concentration of the K+ and Lactate Dehydrogenase(LDH) and the expression of AQPs were detected.ResultsThe miR-29a expression increased in IBS-D control group(2.090±0.022) compared with the control group(1.00±0.031) (P<0.001) while it decreased in IBS-D+miR-29a antagomir group(1.403±0.042) compared with IBS-D control group(P<0.001). The K+ decreased in IBS-D control group(1.305±0.289) compared with the control group(2.171±0.204)(P<0.05) while it increased in IBS-D+miR-29a antagomir group(1.813±0.102)(P<0.05) compared with IBS-D control group. The LDH increased in IBS-D control group(4153.440±177.365) compared with the control group(1434.573±96.111)(P<0.001) while it decreased in IBS-D+miR-29a antagomir group(2700.473±275.414) compared with IBS-D control group (P<0.01). The expression of AQP1, AQP3 and AQP8 decreased in IBS-D control group(0.132±0.010,0.110±0.005,0.108±0.007) compared with the control group (P<0.001) while it increased in IBS-D+miR-29a antagomir group(0.197±0.005,0.182±0.011,0.194±0.003) compared with IBS-D control group(P<0.001). The IBS-D+miR-29a negative control(NC) group, a comparison with IBS-D+miR-29a antagomir group, each date showed the similar trend to the IBS-D control group.ConclusionsMiR-29a increased the intestinal membrane permeability of colonic epithelial cells by reducing the AQPs expression in IBS-D rats.

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats

et al. 2017

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“…It has been reported that differential expression of several miRNAs may be correlated with inflammation [29], peripheral circulation [30], immunomodulatory [31], gut microbiota [32], and other processes that are involved in the pathogenesis of IBS-D. For example, Bitar [31] found that miR-155 was expressed in the duodenal epithelium at the acute stage of cholera and could limit the innate immune response of the host, including the inflammation evoked by its own secreted factors. Mansour’s research [32] showed that decreased expression of miR-199b would lead to an increased coliform count. Furthermore, a recent study [33] showed that miR-16 and miR-125b are involved in barrier function dysregulation through the modulation of claudin-2 and cingulin expression in the jejunum in IBS with diarrhoea, which is similar to our research.…”

Section: Discussionmentioning

confidence: 99%

MiR-144 Increases Intestinal Permeability in IBS-D Rats by Targeting OCLN and ZO1

Hou

Huang

Zhu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Irritable bowel syndrome with diarrhoea (IBS-D) is a chronic, functional bowel disorder characterized by abdominal pain or diarrhoea and altered bowel habits, which correlate with intestinal hyperpermeability. MicroRNAs (miRNAs) are involved in regulating intestinal permeability in IBS-D. However, the role of miRNAs in regulating intestinal permeability and protecting the epithelial barrier remains unclear. Our goals were to (i) identify differential expression of miRNAs and their targets in the distal colon of IBS-D rats; (ii) verify in vitro whether occludin (OCLN) and zonula occludens 1 (ZO1/TJP1) were direct targets of miR-144 and were down-regulated in IBS-D rats; and (iii) determine whether down-regulation of miR-144 in vitro could reverse the pathological hallmarks of intestinal hyperpermeability via targeting OCLN and ZO1. Methods: The IBS-D rat model was established using 4% acetic acid and evaluated by haematoxylin-eosin (HE) staining. The distal colon was obtained in order to perform miRNA microarray analysis and to isolate and culture colonic epithelial cells. When differential expression of miRNA was found, the results were verified by qRT-PCR, and the target genes were further explored by bioinformatics analysis. Correlation analyses were carried out to compare the expression of miRNA and target genes. Then, mutants, miRNA mimics and inhibitors of the target genes were constructed and transfected to colonic epithelial cells. qRT-PCR, western blotting, enzyme-linked immunosorbent assays (ELISAs) and dual-luciferase assays were used to investigate the expression of miR-144 and OCLN, ZO1 in IBS-D rats. Results: There were 8 up-regulated and 18 down-regulated miRNAs identified in the IBS-D rat model. Of these, miR-144 was markedly up-regulated and resulted in the down-regulation of OCLN and ZO1 expression. Overexpression of miR-144 by transfection of miR-144 precursor markedly inhibited the expression of OCLN and ZO1. Further studies confirmed that OCLN and ZO1 were direct targets of miR-144. Additionally, intestinal hyperpermeability was enhanced by miR-144 up-regulation and attenuated by miR-144 down-regulation in IBS-D rat colonic epithelial cells. Moreover, rescue experiments showed that overexpression of OCLN and ZO1 significantly eliminated the inhibitory effect of miR-144, which showed a stronger effect on the attenuation of intestinal hyperpermeability. Conclusion: Up-regulation of miR-144 could promote intestinal hyperpermeability and impair the protective effect of the epithelial barrier by directly targeting OCLN and ZO1. miR-144 is likely a key regulator of intestinal hyperpermeability and could be a potential therapeutic target for IBS-D.

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“…Visceral hypersensitivity, the increased sensitivity to colonic distension, has been identified in 33–65% of patients with IBS and considered to be an important pathophysiological mechanism . In addition, previous studies have also shown that miRNAs are of great importance to the process of IBS, including miR‐29a and miR‐199b . Thus, our study tries to investigate the role of miR‐495 in the development of IBS‐D.…”

Section: Discussionmentioning

confidence: 98%

microRNA‐495 reduces visceral sensitivity in mice with diarrhea‐predominant irritable bowel syndrome through suppression of the PI3K/AKT signaling pathway via PKIB

Fei

Wang

2020

IUBMB Life

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Diarrhea‐predominant irritable bowel syndrome (IBS‐D) is one of the most common gastrointestinal disorders in the world, lacking effective therapies. The crucial roles of microRNAs (miRNAs) in IBS‐D have attracted increasing attention. The aim of this study is to investigate the effects of miR‐495 on the visceral sensitivity of the IBS‐D through the PI3K/AKT signaling pathway by targeting PKIB. Microarray data analysis was employed to screen the differentially expressed genes related to IBS‐D and regulatory miRNAs. Then, mice were perfused with acetic acid into the rectum to establish the IBS‐D model. Next, PKIB expression was measured in IBS‐D mice. Additionally, model mice were injected with a series of adenovirus vector to investigate the influence of miR‐495 on visceral sensitivity and rectal function in IBS‐D mice with the involvement of PKIB and PI3K/AKT signaling pathway. The IBS‐D mouse model was successfully established. PKIB was the target gene of miR‐495, and highly expressed in mice with IBS‐D. Silencing PKIB reduced visceral sensitivity in mice with IBS‐D, and overexpression of miR‐495 decreased visceral sensitivity in mice with IBS‐D by inhibiting PKIB. Moreover, miR‐495 upregulation inhibited PI3K/AKT signaling pathway through downregulating PKIB. To sum up, this study reveals that miR‐495 upregulation can reduce visceral sensitivity in IBS‐D via inhibition of PI3K/AKT signaling pathway by targeting PKIB. It suggests that miR‐495 presents a potential target for IBS‐D therapy.

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MicroRNA‐199b expression level and coliform count in irritable bowel syndrome

Cited by 11 publications

References 42 publications

MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats

MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats

MiR-144 Increases Intestinal Permeability in IBS-D Rats by Targeting OCLN and ZO1

microRNA‐495 reduces visceral sensitivity in mice with diarrhea‐predominant irritable bowel syndrome through suppression of the PI3K/AKT signaling pathway via PKIB

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