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Updated: Aug 16, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
Published on: June 29, 2012
Autocrine release of TGF-beta by portal fibroblasts regulates cell growth
Rebecca G Wells1, Emma Kruglov, Jonathan A Dranoff
1The University of Pennsylvania School of Medicine, 600 CRB/6140, 415 Curie Blvd., Philadelphia, PA 19104-6140, USA. rgwells@mail.med.upenn.edu
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.
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