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Commentary
Chemokines in colitis: microRNA control
  1. Ishan Roy1,
  2. Christopher T Veldkamp2,
  3. Brian F Volkman3,
  4. Michael B Dwinell1
  1. 1 Department of Microbiology & Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
  2. 2 Department of Chemistry, University of Wisconsin-Whitewater, Whitewater, Wisconsin, USA
  3. 3 Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
  1. Correspondence to Dr Michael B Dwinell, Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA; mdwinell{at}mcw.edu

https://doi.org/10.1136/gutjnl-2013-305886

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    Huang et al 1 identified and tested the role of a specific microRNA (miRNA) in the pathogenesis of IBD. The study of microRNAs is a burgeoning field within epigenetics. These small non-coding RNAs mediate translation-level repression of protein expression by binding to the 3′ -untranslated region of specific messenger RNA transcripts. In the innate and adaptive immune response, miRNAs play an important role in negative regulation of inflammatory conditions in the intestine. Inflammatory regulators such as IL-6, tumor necrosis factor (TNF) and toll-like receptors have been shown to induce miRNA expression in both acute and chronic inflammation. The roles for miRNAs in IBD are emerging from recent studies that compare miRNA expression in colonoscopic and peripheral blood draw biopsies from colitis patients with healthy individuals.2 Despite this, the vast majority of miRNAs identified in microarray analyses of colitis patients have yet to be investigated in experimental models of colitis or assigned specific mechanisms in the pathophysiology of human disease. In a novel approach, Huang et al 1 used array analyses to assay changes in microRNA expression from two different experimental models of colitis in order to map specific overlapping miRNA expression patterns, which were subsequently compared against analyses completed on human colitis patient specimens. These authors then continued their analyses to mechanistically determine that miR-141, a miRNA aberrantly expressed in both animal models of colitis and human patients, specifically inhibited expression of the β-isoform of CXCL12, a …

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    Footnotes

    • Contributors IR and MBD wrote the initial drafts of the commentary. CTV and BFV edited the initial draft and provided information on chemokine structure to the commentary.

    • Competing interests The use of recombinant CXCL12 as an antimetastatic drug is protected by US Patent 8 404 640 to MBD. BFV and MBD as co-founders of Protein Foundry, LLC, a manufacturer of molecular grade chemokines for use in biomedical research.

    • Provenance and peer review Commissioned; internally peer reviewed.

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