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Connective tissue growth factor expression is increased in collagenous colitis and coeliac disease
Author(s) -
Günther Ute,
Bateman Adrian C,
Beattie R Mark,
Bauer Michael,
MacDonald Thomas T,
Kaskas Berndt A
Publication year - 2010
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2010.03652.x
Subject(s) - coeliac disease , ctgf , collagenous colitis , connective tissue , pathology , ulcerative colitis , medicine , histopathology , inflammatory bowel disease , fibrosis , colitis , growth factor , biology , disease , receptor
Günther U, Bateman A C, Beattie R M, Bauer M, MacDonald T T & Kaskas B A
(2010) Histopathology 57 , 427–435
Connective tissue growth factor expression is increased in collagenous colitis and coeliac disease Aims: Subepithelial collagen deposition is a classical feature of collagenous colitis (CC), but is also seen in untreated coeliac disease. The end‐stage mediator of excess cellular collagen production is connective tissue growth factor (CTGF). The aim of this study was to investigate CTGF expression by in situ hybridization (ISH) and polymerase chain reaction (PCR) in CC and coeliac disease as well as lymphocytic colitis (LC), Crohn’s colitis and ulcerative colitis (UC). Methods and results: For coeliac disease we analysed fresh frozen material by quantitative reverse transcription–polymerase chain reaction (RT–PCR) and archival material for ISH. PCR transcripts in coeliac disease were moderately elevated and labelled cells were significantly increased in the subepithelial zone. For CC, LC and UC we investigated archival material because of the rarity of the first two conditions. There was a marked increase in CTGF expression in the subepithelial zone in CC, localizing to cells with the morphology of smooth muscle cells, which was not seen in LC. Conclusions: The colocalization of CTGF transcripts with areas of excessive collagen deposition in coeliac disease and CC suggest that it might be the end‐stage mediator of local fibrosis in these conditions.