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1: Biochem Biophys Res Commun. 2007 Sep 21;361(2):335-41. Epub 2007 Jul 24.

Expression and function of fibroblast growth factor (FGF) 9 in hepatic stellate
cells and its role in toxic liver injury.

Antoine M, Wirz W, Tag CG, Gressner AM, Marvituna M, Wycislo M, Hellerbrand C,
Kiefer P.

Institute of Clinical Chemistry and Laboratory Medicine, University of
Regensburg, Franz-Josef-Strauss-Allee 11, D-93042 Regensburg, Germany.

Hepatic injury and regeneration of the liver are associated with activation of
hepatic stellate cells (HSC). Fibroblast growth factors (FGFs) and their
receptors are important regulators of repair in various tissues. HSC express
FGFR3IIIc as well as FGFGR4 and different spliced FGFR1IIIc and FGFR2IIIc
isoforms which differ in the presence or absence of the acid box and of the first
Ig-like domain. Expression of FGF9, known to be capable to activate the HSC
FGFR2/3-isoforms, was increased in HSC in liver slice cultures after exposition
to carbon tetrachloride, as an acute liver injury model. FGF9 significantly
stimulated 3-H thymidine incorporation of hepatocytes, but failed to induce DNA
synthesis in HSC despite the fact that FGF9 induced a sustained activation of
extracellular signal-related kinases (ERK) 1/2. FGF9 induced an increased
phosphorylation of Tyr436 of the fibroblast growth factor receptor substrate
(FRS) 2, while phosphorylation of Tyr196 which is required for efficient Grb2
recruitment remained unchanged. Our findings suggest that HSC FGF9 provide a
paracrine mitogenic signal to hepatocytes during acute liver injury, while the
autocrine FGF9 signaling appears to be not sufficient to induce cell
proliferation.

PMID: 17662249 [PubMed - indexed for MEDLINE]

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