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Focal Up-Regulation of E-Cadherin-Catenin Complex in Inflamed Bowel Mucosa but Reduced Expression in Ulcer-Associated Cell Lineage
Author(s) -
Pieter Demetter,
Martine De Vos,
Nancy Van Damme,
Dominique Baeten,
Dirk Elewaut,
Stefan Vermeulen,
Marc Mareel,
Gillian Bullock,
Herman Mielants,
Gust Verbruggen,
Filip De Keyser,
Eric Veys,
Claude Cuvelier
Publication year - 2000
Publication title -
american journal of clinical pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.859
H-Index - 128
eISSN - 1943-7722
pISSN - 0002-9173
DOI - 10.1093/ajcp/114.3.364
Subject(s) - cadherin , epithelium , biology , inflammation , pathology , cell adhesion molecule , intestinal epithelium , beta catenin , immunohistochemistry , microbiology and biotechnology , cell , immunology , medicine , signal transduction , wnt signaling pathway , genetics
The E-cadherin-catenin complex is important for the maintenance of epithelial architecture. We studied its expression in Crohn disease, ulcerative colitis, acute ileitis, and controls. Immunohistochemical stainings for E-cadherin, alpha-catenin, beta-catenin and gamma-catenin were performed. E-cadherin messenger RNA (mRNA) was detected using riboprobes. In active inflammation, there was up-regulation of the complex. In particular, epithelium adjacent to ulcers showed increased expression of protein and mRNA, but in ulcer-associated cell lineage, the intensity of staining was weak to negative. In focal inflammation, up-regulation was found in affected areas. Reparative epithelium growing over denuded areas showed weaker expression. Since structural or functional perturbation in any of the molecules of the E-cadherin-catenin complex results in loss of intercellular adhesion, the preexistent epithelium may benefit from up-regulation to try to maintain its normal architecture under inflammatory conditions. Reduced expression in reparative epithelium and ulcer-associated cell lineage could facilitate the motility of these cells.

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