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In situ expression of fibrogenic growth factors and their receptors in biliary atresia: comparison between early and late stages
Author(s) -
Faiz Kabir Uddin Ahmed Abul,
Ohtani Haruo,
Nio Masaki,
Funaki Nobuo,
Iwami Daiji,
Kumagai Shinji,
Sato Eiichi,
Nagura Hiroshi,
Ohi Ryoji
Publication year - 2000
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/1096-9896(2000)9999:9999<::aid-path657>3.0.co;2-j
Subject(s) - biliary atresia , autocrine signalling , paracrine signalling , receptor , fibrosis , platelet derived growth factor receptor , myofibroblast , bile duct , immunohistochemistry , biology , medicine , atresia , endocrinology , pathology , cancer research , growth factor , transplantation , liver transplantation
Progressive fibrosis, despite successful surgical treatment, is one of the serious complications of biliary atresia. To understand the mechanism of this fibrosis, the in situ expression of fibrogenic growth factors (TGF‐β and PDGF) and their corresponding receptors was studied by immunohistochemistry using frozen sections. The results were compared between the early ( n =12) and late ( n =6) stages. The early stage was characterized by abundant expression of all ligands and receptors, together with type I procollagen (PC‐I). The major cellular sources were activated fibroblasts/myofibroblasts distributed mostly in the portal tracts. Macrophages also expressed all the ligands and the receptors, but to a lesser degree. Bile duct cells strongly expressed TGF‐β RI and RII and PDGF AA and BB, but focally expressed TGF‐β. All of these decreased in the late stage of biliary atresia. These results suggest that TGF‐β and PDGF play important roles in the fibrogenesis of biliary atresia, especially in its early stage, acting either by autocrine or paracrine mechanisms involving activated fibroblasts/myofibroblasts, bile duct cells, and macrophages. Copyright © 2000 John Wiley & Sons, Ltd.