Regulation of antiapoptotic and cytoprotective pathways in colonic epithelial cells in ulcerative colitis

摘要: Ulcerative colitis is an inflammatory bowel disease involving the colon resulting in bloody diarrhea and increased risk of colorectal cancer certain patient subgroups. Increased apoptosis epithelial cell layer causes permeability, especially during flares; this leads to translocation luminal pathogens a continued drive. The present work investigates how regulated ulcerative colitis. main results are that Fas mediated inhibited flares colitis, probably by upregulation cellular inhibitor protein 2 (cIAP2) FLICE-like inhibitory protein. cIAP2 upregulated regenerative cells both experimental intestinal wounds. Inhibition decreases wound healing vitro possibly through inhibition migration. Altogether, it shown responds hostile microenvironment activation cytoprotective pathways tend counteract cytotoxic effects inflammation. However, studies also show produce amounts reactive oxygen species stimulation with tumor necrosis factor-α interferon-γ DNA instability. combined effect DNA-instability decreased responses could lead neoplasia.