TY - JOUR T1 - Chemokines in colitis: microRNA control JF - Gut JO - Gut SP - 1202 LP - 1204 DO - 10.1136/gutjnl-2013-305886 VL - 63 IS - 8 AU - Ishan Roy AU - Christopher T Veldkamp AU - Brian F Volkman AU - Michael B Dwinell Y1 - 2014/08/01 UR - http://gut.bmj.com/content/63/8/1202.abstract N2 - 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 … ER -