Role of far upstream element binding protein 1 in colonic epithelial disruption during dextran sulphate sodium-induced murine colitis.
Year: 2014
Type: article
Abstract: AIM: Intestinal epithelial barrier is essential for maintaining normal intestinal homeostasis; its breakdown leads to chronic inflammatory pathologies, such as inflammatory bowel diseases. Far upstream element binding protein 1 (FBP1) has been reported to play an important role in cell apoptosis and proliferation. We aimed to investigate the expression and the role of FBP1 in dextran sodium sulphate (DSS)-induced experimental colitis. METHODS: Mice experimental colitis model was established by administration of DSS, and the expression and localization of FBP1 was examined using Western blot and immunohistochemistry. Colon epithelial cell line HT-29 was used to determine the role of FBP1. In vitro study, the expression of FBP1 was determined in HT-29 cells stimulated with tumor necrosis factor α (TNF-α). HT-29 cells were transfected with FBP1 siRNA and then measured for viability. RESULTS: Significant decreasing of FBP1 expression was found in mice colitis. In addition, FBP1 was cleaved and translocated from nucleus to cytoplasm during apoptosis. Downregulated expression of FBP1 induced cell cycle arrest. CONCLUSIONS: We demonstrate that apoptosis-mediated cleavage of FBP1 and its decreased expression in epithelial cells induces cell cycle arrest, which may play an important role in colonic epithelial disruption.
Source: PubMed Central
Authors: Qiyun Tang, Weiwei Xia, Qianqian Ji, Runzhou Ni, Jian'an Bai, Liren Li, Yongwei Qin
Language: English
Topic: Inflammatory Bowel Disease
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2216979982