Autocrine release of TGF‐β by portal fibroblasts regulates cell growth

FEBS Letters

Kruglov, Emma¹  Dranoff, Jonathan A¹  Wells, Rebecca G² 

[1] Yale University School of Medicine, New Haven, CT, USA;The University of Pennsylvania School of Medicine, 600 CRB/6140, 415 Curie Blvd., Philadelphia, PA 19104-6140, USA

关键词: Transforming growth factor-β;    Transforming growth factor-β receptor;    Betaglycan;    Fibrosis;    Biliary cirrhosis;    Portal fibroblast;    TGF-β;    transforming growth factor-β;    PF;    portal fibroblasts;    HSC;    hepatic stellate cells;    FGF;    fibroblast growth factor;    PDGF;    platelet derived growth factor;    TβRI;    type I TGF-β receptor;    TβRII;    type II TGF-β receptor;   

DOI  :  10.1016/S0014-5793(04)00037-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown