Regulation of epithelial syndecan-1 expression by inflammatory cytokines

Day, Richard M, Mitchell, Tracey J, Knight, Stella C and Forbes, Alastair (2003) Regulation of epithelial syndecan-1 expression by inflammatory cytokines. Cytokine, 21 (5). pp. 224-33. ISSN 1043-4666

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Abstract

Syndecan-1 is expressed on the basolateral surface of columnar epithelium and contributes to wound repair by facilitating increased growth factor binding. Inflammatory bowel disease (IBD) is associated with reduced syndecan-1 expression in areas of inflamed mucosa that is likely to impair mucosal healing. Reduced syndecan-1 expression in IBD may be related to the presence of increased inflammatory cytokines. To test this hypothesis, monolayers of HT29 and T84 colonic epithelial cells were stimulated with tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta or IL-6. Stimulation of HT29 cells with TNF-alpha and IL-1beta resulted in reversible down-regulation of syndecan-1 at both protein and mRNA levels but little effect was observed with IL-6. Loss of syndecan-1 expression was caused by shedding of the ectodomain as revealed by increased levels of soluble syndecan-1 measured in the conditioned medium of stimulated cells. No increase in cytoplasmic staining accompanied the loss of cell surface syndecan-1 expression. TNF-alpha and IL-1beta are capable of down-regulating syndecan-1 expression and may account in part for the reduced expression of syndecan-1 seen in IBD.

Item Type: Article
Uncontrolled Keywords: cells, cultured,coculture techniques,cytokines,epithelial cells,gene expression regulation,humans,intercellular adhesion molecule-1,interleukin-1,interleukin-6,leukocytes, mononuclear,membrane glycoproteins,protein structure, tertiary,proteoglycans,rna, messenger,syndecan-1,syndecans,tumor cells, cultured,tumor necrosis factor-alpha
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
Depositing User: Pure Connector
Date Deposited: 06 Aug 2014 11:40
Last Modified: 11 Apr 2019 15:41
URI: https://ueaeprints.uea.ac.uk/id/eprint/49586
DOI:

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