Mechanisms of epithelial cell shedding in the Mammalian intestine and maintenance of barrier function

Watson, Alastair J M ORCID:, Duckworth, Carrie A, Guan, Yanfang and Montrose, Marshall H (2009) Mechanisms of epithelial cell shedding in the Mammalian intestine and maintenance of barrier function. Annals of the New York Academy of Sciences, 1165. pp. 135-142. ISSN 1749-6632

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The intestinal epithelium forms a barrier between the gut lumen and the body. The barrier is potentially challenged by the high turnover of epithelial cells being shed. Our laboratories have shown that the epithelium is punctuated by discontinuities called "gaps" that have the diameter of an epithelial cell and are devoid of cellular contents. At least a proportion of gaps are formed by the shedding of epithelial cells. These gaps are filled with an unknown substance that maintains local barrier function. Gaps have been identified in the mouse by in vivo confocal microscopy and in humans by confocal endomicroscopy. They can be distinguished from goblet cells by the absence of a nucleus and are found in Math1-/- mice where goblet cells are absent. Cell shedding and gap formation is increased by TNF-alpha. Barrier function is lost after TNF-alpha in approximately 20% of shedding events. These observations suggest that loss of barrier function at sites of cell shedding may be important in intestinal diseases where an increase in epithelial permeability plays a role in pathogenesis.

Item Type: Article
Uncontrolled Keywords: animals,basic helix-loop-helix transcription factors,caspase 3,cell membrane permeability,cell movement,epithelial cells,humans,intestinal mucosa,kinetics,mice,microscopy, electron, scanning,tumor necrosis factor-alpha
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups: Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology
Depositing User: EPrints Services
Date Deposited: 25 Nov 2010 11:13
Last Modified: 20 Aug 2023 00:20
DOI: 10.1111/j.1749-6632.2009.04027.x

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