Autocrine release of TGF-beta by portal fibroblasts regulates cell growth.

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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@article{Wells2004AutocrineRO, title={Autocrine release of TGF-beta by portal fibroblasts regulates cell growth.}, author={Rebecca G Wells and Emma A Kruglov and Jonathan A. Dranoff}, journal={FEBS letters}, year={2004}, volume={559 1-3}, pages={107-10} }