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Role of miR-150-targeting c-Myb in Colonic Epithelial Disruption During Dextran Sulphate Sodium-Induced Murine Experimental Colitis and Human Ulcerative Colitis

Role of miR-150-targeting c-Myb in Colonic Epithelial Disruption During Dextran Sulphate Sodium-Induced Murine Experimental Colitis and Human Ulcerative Colitis

Zhen Bian, Limin Li, Jinglong Cui, Hongjie Zhang, Yuan Liu, Chen-Yu Zhang, Ke Zen

J Pathol. 2011 Dec;225(4):544-53.

PMID: 21590770

Abstract:

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

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42412573	Bcl-2 Active human			Price

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