MiR‐155 promotes colitis‐associated intestinal fibrosis by targeting HBP1/Wnt/β‐catenin signalling pathway

• Published in: Journal of cellular and molecular medicine Vol. 25; no. 10; pp. 4765 - 4775
• Main Authors: Li, Nianshuang, Ouyang, Yaobin, Xu, Xinbo, Yuan, Zhenxiang, Liu, Chunquan, Zhu, Zhenhua
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.05.2021; John Wiley and Sons Inc
• Subjects: Antibodies; Binding sites; Catenin; Cell cycle; Cell growth; Colitis; Collagen; Colon; Crohn's disease; Disease; Ethanol; Fibroblasts; Fibrosis; Gene expression; HBP1; Homeostasis; Inflammation; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory diseases; intestinal fibrosis; Intestine; Liver; Liver cirrhosis; Lung cancer; MicroRNAs; miRNA; miR‐155; Original; Proteins; Signal transduction; Stricture; Wnt protein; Wnt/β‐catenin signalling pathway; Wound healing; β-Catenin; Crohn's disease; HBP1; Wnt/β-catenin signalling pathway; intestinal fibrosis; miR-155
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/jcmm.16445

Intestinal fibrosis is the most common complication of Crohn's disease (CD) that is one major disorder of inflammatory bowel disease (IBD), but the precise mechanism remains unclear. MiR‐155 has been involved in fibrotic diseases. Here, we determined the role of miR‐155 in regulating intestinal fibrosis. MiR‐155 levels were significantly up‐regulated in CD patients with intestinal stricture CD. The overexpression of miR‐155 significantly aggravated TNBS‐induced CD‐associated intestinal fibrosis. Mechanistically, we identified that HBP1, a negative regulator of the Wnt/β‐catenin signalling pathway, is a direct target of miR‐155. Moreover, in vitro and in vivo experiments suggested that the miR‐155/HBP1 axis activates Wnt/β‐catenin signalling pathway to induce intestinal fibrosis. Taken together, we demonstrated that miR‐155 directly targets HBP1 to induce CD‐associated intestinal fibrosis via Wnt/β‐catenin signalling pathway.