Regulation of intestinal epithelial gene expression in hypoxia.
Mucosal hypoxia is intimately associated with chronic inflammation in the gastrointestinal tract in disease such as Crohn's disease. Under such conditions, intestinal epithelial cells may become a source of proinflammatory cytokines, including tumor necrosis factor alpha (TNFalpha), which actively contribute to ongoing inflammation through autocrine disruption of epithelial barrier function. These events are critically dependent upon alterations in the expression and function of the cAMF response element binding protein (CREB). Here we review our understanding of the molecular mechanisms underlying the regulation of CREB activity in intestinal epithelial cells in hypoxia.
Taylor
Cormac T
CT
Dept. Medicine and Therapeutics, The Conway Institute, University College, Dublin, Ireland. cormac.taylor@ucd.ie
D000818:Animals; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D017362:Cyclic AMP Response Element-Binding Protein; D014409:Tumor Necrosis Factor-alpha