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

Antoine, Marianne; Wirz, W.; Tag, Carmen G.; Gressner, A. M.; Marvituna, Meltem; Wycislo, M.; Hellerbrand, Claus; Kiefer, Paul

doi:10.1016/j.bbrc.2007.06.189

Cited by 38 publications

(60 citation statements)

References 11 publications

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“…PDGF stimulates the Ras/ERK signaling pathways during liver fibrogenesis (35). It is well known that the ERK/MAPK signaling pathway is involved in cell growth, differentiation, and migration of HSCs during liver fibrosis and cirrhosis (2,43). What is more, the PI3K-Akt signaling pathway promotes cell proliferation and collagen gene expression by inhibition of apoptosis in HSCs (15).…”

Section: Discussionmentioning

confidence: 99%

Fluorofenidone attenuates hepatic fibrosis by suppressing the proliferation and activation of hepatic stellate cells

Yang

Wang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 99%

Fluorofenidone attenuates hepatic fibrosis by suppressing the proliferation and activation of hepatic stellate cells

Yang

Wang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Therefore, FGF1 may not have an essential role in liver mass restoration. Increased expression of FGF9 in activated HSCs provides a mitogenic signal to hepatocytes in the liver, which is insulted by CCl 4 [9]. Expression of FGF21 is up-regulated in hepatocytes during liver regeneration after PH or CCl 4 administration, but overexpression of FGF21 does not affect compensatory growth after either treatment [10].…”

Section: Introductionmentioning

confidence: 97%

Expression and Function of Fibroblast Growth Factor (FGF) 7 during Liver Regeneration

Tsai

Wang

2011

Cell Physiol Biochem

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Background/Aim: Previous studies have shown that fibroblast growth factors (FGFs) are involved in the process of liver injury repair. Liver regeneration after partial hepatectomy (PH) is impaired in transgenic mice expressing dominant-negative FGFR2b in hepatocytes. Although FGF7, a ligand specifically bound to FGFR2b, is expressed by activated hepatic stellate cells (HSCs) in fibrotic livers, the expressions and functions of FGF7 and FGFR2b after PH remain unexplored. Therefore, this study sought to examine the potential role of FGF7 signaling during liver regeneration. Methods: We examined the expression of FGF7 and FGFR2b in normal and regenerating livers. Effects of FGF7 on hepatocytes were examined in vitro using primary hepatocyte culture with FGF7 recombinant protein and in vivo by hydrodynamic-based gene transfer method. Results: We found that FGF7 expression was increased according to the activation status of HSCs after PH. The receptor, FGFR2b, was also increased in hepatocytes during liver regeneration. In vitro treatment with FGF7 protein activated ERK1/2 and promoted proliferation of hepatocytes isolated from regenerating livers. In vivo overexpression of exogenous FGF7 could notably promote hepatic proliferation and activate MAPKs after PH. Conclusion: This study suggests a role for activated HSC-expressed FGF7 in stimulating FGF signaling pathways in hepatocytes and regulating liver regeneration.

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“…In the chick embryo, BMP and FGF signaling induce hepatic genes in the endoderm, as is the case in the mouse (Zhang et al, 2004). However, the involvement of these factors in later hepatic development has not been established, although it has been reported that several members of the FGF family are expressed in adult liver and involved in hepatocyte proliferation (Antoine et al, 2006(Antoine et al, , 2007.…”

Section: Introductionmentioning

confidence: 99%

FGF signaling segregates biliary cell‐lineage from chick hepatoblasts cooperatively with BMP4 and ECM components in vitro

Yanai

Tatsumi

Hasunuma

et al. 2008

Developmental Dynamics

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Intrahepatic bile ducts (IHBDs) are indispensable for transporting bile secreted from hepatocytes to the hepatic duct. The biliary epithelial cells (BECs) of the IHBD arise from bipotent hepatoblasts around the portal vein, suggesting the portal mesenchyme is essential for their development. However, except for Notch or Activin/ TGF-␤ signaling molecules, it is not known which molecules regulate IHBD development. Here, we found that FGF receptors and BMP4 are specifically expressed in the developing IHBD and the hepatic mesenchyme, respectively. Using a mesenchyme-free culture of liver bud, we showed that bFGF and FGF7 induce the hepatoblasts to differentiate into BECs, and that BMP4 enhances bFGF-induced BEC differentiation. The extracellular matrix (ECM) components in the hepatic mesenchyme induced BEC differentiation. Forced expression of a constitutively active form of the FGF receptor partially induced BEC differentiation markers in vivo. These data strongly suggest that bFGF and FGF7 promote BEC differentiation cooperatively with BMP4 and ECMs in vivo.

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

Cited by 38 publications

References 11 publications

Fluorofenidone attenuates hepatic fibrosis by suppressing the proliferation and activation of hepatic stellate cells

Fluorofenidone attenuates hepatic fibrosis by suppressing the proliferation and activation of hepatic stellate cells

Expression and Function of Fibroblast Growth Factor (FGF) 7 during Liver Regeneration

FGF signaling segregates biliary cell‐lineage from chick hepatoblasts cooperatively with BMP4 and ECM components in vitro

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