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      MicroRNAs: new players in IBD

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          Abstract

          MicroRNAs (miRNAs) are small non-coding RNAs, 18–23 nucleotides long, which act as post-transcriptional regulators of gene expression. miRNAs are strongly implicated in the pathogenesis of many common diseases, including IBDs. This review aims to outline the history, biogenesis and regulation of miRNAs. The role of miRNAs in the development and regulation of the innate and adaptive immune system is discussed, with a particular focus on mechanisms pertinent to IBD and the potential translational applications.

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          Most cited references125

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          Switching from repression to activation: microRNAs can up-regulate translation.

          Shobha Vasudevan, Yingchun Tong, Joan Steitz (2007)
          AU-rich elements (AREs) and microRNA target sites are conserved sequences in messenger RNA (mRNA) 3' untranslated regions (3'UTRs) that control gene expression posttranscriptionally. Upon cell cycle arrest, the ARE in tumor necrosis factor-alpha (TNFalpha) mRNA is transformed into a translation activation signal, recruiting Argonaute (AGO) and fragile X mental retardation-related protein 1 (FXR1), factors associated with micro-ribonucleoproteins (microRNPs). We show that human microRNA miR369-3 directs association of these proteins with the AREs to activate translation. Furthermore, we document that two well-studied microRNAs-Let-7 and the synthetic microRNA miRcxcr4-likewise induce translation up-regulation of target mRNAs on cell cycle arrest, yet they repress translation in proliferating cells. Thus, activation is a common function of microRNPs on cell cycle arrest. We propose that translation regulation by microRNPs oscillates between repression and activation during the cell cycle.
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            Network motifs in the transcriptional regulation network of Escherichia coli

            Shai S Shen-Orr, Ron Milo, Shmoolik Mangan … (2002)
            Little is known about the design principles of transcriptional regulation networks that control gene expression in cells. Recent advances in data collection and analysis, however, are generating unprecedented amounts of information about gene regulation networks. To understand these complex wiring diagrams, we sought to break down such networks into basic building blocks. We generalize the notion of motifs, widely used for sequence analysis, to the level of networks. We define 'network motifs' as patterns of interconnections that recur in many different parts of a network at frequencies much higher than those found in randomized networks. We applied new algorithms for systematically detecting network motifs to one of the best-characterized regulation networks, that of direct transcriptional interactions in Escherichia coli. We find that much of the network is composed of repeated appearances of three highly significant motifs. Each network motif has a specific function in determining gene expression, such as generating temporal expression programs and governing the responses to fluctuating external signals. The motif structure also allows an easily interpretable view of the entire known transcriptional network of the organism. This approach may help define the basic computational elements of other biological networks.
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              Nuclear export of microRNA precursors.

              Elsebet Lund, Stephan Güttinger, Angelo Calado … (2004)
              MicroRNAs (miRNAs), which function as regulators of gene expression in eukaryotes, are processed from larger transcripts by sequential action of nuclear and cytoplasmic ribonuclease III-like endonucleases. We show that Exportin-5 (Exp5) mediates efficient nuclear export of short miRNA precursors (pre-miRNAs) and that its depletion by RNA interference results in reduced miRNA levels. Exp5 binds correctly processed pre-miRNAs directly and specifically, in a Ran guanosine triphosphate-dependent manner, but interacts only weakly with extended pre-miRNAs that yield incorrect miRNAs when processed by Dicer in vitro. Thus, Exp5 is key to miRNA biogenesis and may help coordinate nuclear and cytoplasmic processing steps.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Gut
                Journal ID (iso-abbrev): Gut
                Journal ID (hwp): gutjnl
                Journal ID (publisher-id): gut
                Title: Gut
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Print): 0017-5749
                ISSN (Electronic): 1468-3288
                Publication date (Print): March 2015
                Publication date (Electronic): 4 December 2014
                Volume: 64
                Issue: 3
                Pages: 504-513
                Affiliations
                [1 ]Gastrointestinal Unit, Centre for Molecular Medicine, Institute of Genetics and Molecular Medicine, Western General Hospital , Edinburgh, UK
                [2 ]Centre for Immunity, Infection and Evolution, Ashworth laboratories, University of Edinburgh , Edinburgh, UK
                Author notes
                [Correspondence to ] Professor Jack Satsangi, Gastrointestinal Unit, Western General Hospital, Crewe Road South, Edinburgh EH4 2XU, UK; j.satsangi@ 123456ed.ac.uk
                Article
                Publisher ID: gutjnl-2014-307891
                DOI: 10.1136/gutjnl-2014-307891
                PMC ID: 4345829
                PubMed ID: 25475103
                SO-VID: c9d9792f-63e5-4262-a5bc-3f9aa28ad757
                Copyright © Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                Date received : 23 June 2014
                Date revision received : 9 October 2014
                Date accepted : 23 October 2014
                Categories
                Subject: 1239
                Subject: 1506
                Subject: Recent Advances in Basic Science
                Custom metadata
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                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: ulcerative colitis,intestinal tract,crohn's disease,cellular immunology,t lymphocytes
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: ulcerative colitis, intestinal tract, crohn's disease, cellular immunology, t lymphocytes

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