Lastly, analysis of public data from human patients with ulcerative colitis reveals that miR-31 expression is significantly increased when compared to controls.
The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice.
Jun N-terminal kinase inhibition decreased SP-induced miR-31-3p expression. miR-31-3p expression was increased in both TNBS- and DSS-induced colitis and human colonic biopsies from ulcerative colitis, compared with controls.
Furthermore, miR-31 is universally expressed in both ulcerative colitis and Crohn disease not only in fresh-frozen but also in formalin-fixed, paraffin-embedded tissues.