Abstract
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-beta (TGF)-beta is a key growth factor in fibrosis, we characterized the response of PF to TGF-beta. We demonstrate that PF produce significant amounts of TGF-beta2 and, unlike activated hepatic stellate cells (HSC), express all three TGF-beta receptors and are growth inhibited by TGF-beta1 and TGF-beta2. 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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Autocrine Communication / physiology*
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Cell Division / drug effects
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Cells, Cultured
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Fibroblasts / chemistry
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Fibroblasts / cytology*
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Hepatocytes / cytology
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Hepatocytes / metabolism
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Liver / cytology*
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Liver Cirrhosis / etiology
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Liver Cirrhosis / pathology
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Rats
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Receptors, Transforming Growth Factor beta / analysis
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Transforming Growth Factor beta / biosynthesis
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Transforming Growth Factor beta / metabolism
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Transforming Growth Factor beta / pharmacology
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Transforming Growth Factor beta / physiology*
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Transforming Growth Factor beta1
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Transforming Growth Factor beta2
Substances
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Receptors, Transforming Growth Factor beta
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Tgfb1 protein, rat
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Transforming Growth Factor beta
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Transforming Growth Factor beta1
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Transforming Growth Factor beta2