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Autocrine release of TGF‐β by portal fibroblasts regulates cell growth
Author(s) -
Wells Rebecca G,
Kruglov Emma,
Dranoff Jonathan A
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(04)00037-7
Subject(s) - transforming growth factor , hepatic stellate cell , autocrine signalling , growth factor , myofibroblast , platelet derived growth factor , platelet derived growth factor receptor , fibroblast growth factor , cancer research , fibrosis , microbiology and biotechnology , fibroblast , population , biology , endocrinology , receptor , chemistry , medicine , cell culture , genetics , environmental health
Portal fibroblasts (PF) are a newly isolated population of fibrogenic cells in the liver postulated to play a significant role in early biliary fibrosis. Because transforming growth factor‐β (TGF)‐β is a key growth factor in fibrosis, we characterized the response of PF to TGF‐β. We demonstrate that PF produce significant amounts of TGF‐β2 and, unlike activated hepatic stellate cells (HSC), express all three TGF‐β receptors and are growth inhibited by TGF‐β1 and TGF‐β2. Fibroblast growth factor (FGF)‐2, but not platelet derived growth factor (PDGF), causes PF proliferation. These data suggest a mechanism whereby HSC eclipse PF as the dominant myofibroblast population in biliary fibrosis.