Qiyun Tang1, Weiwei Xia2, Qianqian Ji2, Runzhou Ni2, Jian'an Bai1, Liren Li2, Yongwei Qin3. 1. Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University 300 Guangzhou Road, Nanjing 210000, Jiangsu Province, People's Republic of China. 2. Department of Gastroenterology, Affiliated Hospital of Nantong University 20 Xisi Road, Nantong 226001, Jiangsu Province, People's Republic of China. 3. Department of Pathogen Biology, Nantong University Medical College 19 Qixiu Road, Nantong 226001, Jiangsu Province, People's Republic of China.
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.
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 micecolitis. 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.
Authors: Joerg-Dieter Schulzke; Christian Bojarski; Sebastian Zeissig; Frank Heller; Alfred H Gitter; Michael Fromm Journal: Ann N Y Acad Sci Date: 2006-08 Impact factor: 5.691
Authors: Pedro Berraondo; Ignacio Melero; Elisabeth Perez-Ruiz; Luna Minute; Itziar Otano; Maite Alvarez; Maria Carmen Ochoa; Virginia Belsue; Carlos de Andrea; Maria Esperanza Rodriguez-Ruiz; Jose Luis Perez-Gracia; Ivan Marquez-Rodas; Casilda Llacer; Martina Alvarez; Vanesa de Luque; Carmen Molina; Alvaro Teijeira Journal: Nature Date: 2019-05-01 Impact factor: 49.962