Role of miR‐150‐targeting c‐Myb in colonic epithelial disruption during dextran sulphate sodium‐induced murine experimental colitis and human ulcerative colitis

• DOI: 10.1002/path.2907
• Publication Date: 2011-03-29T07:48:51Z
• Authors: Zhen Bian; Limin Li; Jinglong Cui; Hongjie Zhang; Yuan Liu; Chen‐Yu Zhang; Ke Zen
• Keywords: MYB

Chronic inflammatory bowel diseases (IBDs) are associated with differential expression of genes involved in inflammation and tissue remodelling. We surveyed the profile apoptosis-related microRNAs by real-time quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) a dextran sulphate sodium (DSS) murine model colitis. found that miR-150 was strongly elevated, whereas c-Myb, transcription factor target gene miR-150, significantly reduced colon after DSS treatment. Interestingly, elevation down-regulation c-Myb were also observed human active ulcerative colitis compared to normal colon. Supporting observation treatment inducing colonic cell apoptosis, Bcl-2, an anti-apoptotic protein known be regulated DSS-treated mice. Furthermore, forced pre-miR-150 epithelial HT29 cells elevated levels decreased Bcl-2 levels, thus enhancing apoptosis induced serum deprivation. Together, present study presents first evidence its targeting may serve as new mechanism underlying disruption DSS-induced experimental IBD.