scholarly journals Interaction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferation

2016 ◽  
Vol 239 (1) ◽  
pp. 109-121 ◽  
Author(s):  
Annika Wilhelm ◽  
Emma L Shepherd ◽  
Aldo Amatucci ◽  
Mamoona Munir ◽  
Gary Reynolds ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Disease ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Fibrotic Liver ◽  
Fibrotic Liver Disease

scholarly journals Liver X Receptor Signaling Is a Determinant of Stellate Cell Activation and Susceptibility to Fibrotic Liver Disease

2011 ◽  
Vol 140 (3) ◽  
pp. 1052-1062 ◽  
Author(s):  
Simon W. Beaven ◽  
Kevin Wroblewski ◽  
Jiaohong Wang ◽  
Cynthia Hong ◽  
Steven Bensinger ◽  
...  
Keyword(s):  
Liver Disease ◽  
Cell Activation ◽  
Stellate Cell ◽  
Liver X Receptor ◽  
Receptor Signaling ◽  
Fibrotic Liver ◽  
Fibrotic Liver Disease

scholarly journals RNA Sequencing of LX-2 Cells Treated with TGF-β1 Identifies Genes Associated with Early Hepatic Stellate Cell Activation

2021 ◽  
Author(s):  
Jack Carson ◽  
Mark W. Robinson ◽  
Grant A. Ramm ◽  
Geoffrey N. Gobert
Keyword(s):  
Liver Disease ◽  
Rna Sequencing ◽  
Cell Activation ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Signalling Pathways ◽  
Fibrotic Liver ◽  
Pathogen Invasion ◽  
Fibrotic Liver Disease ◽  
Tgf Β1

Abstract Hepatic stellate cells (HSCs) are liver-resident myofibroblast precursors. In chronic liver disease, HSC-derived myofibroblasts are responsible for the production of collagen and, as such, are generally associated with diseases characterised by hepatic fibrosis. HSCs undergo a process of "activation" in response to tissue damage or pathogen invasion, thereby assuming roles in extracellular matrix synthesis, wound healing, and pathogen defence. The process of HSC activation and collagen production is most commonly driven by the cytokine transforming growth factor-β1 (TGF-β1). To investigate the transcriptional impact of TGF-β1 signalling on liver myofibroblasts, RNA sequencing was used to quantitate the biological changes observed in LX-2 cells, an activated human HSC line, following TGF-b1 treatment. In total, 5,258 genes were found to be significantly differentially expressed with a false discovery rate cut-off of < 0.1. The topmost deregulated of these genes included those with known roles in influencing HSC activity, as well as those involved in fibrotic responses in other cell lines and tissues. Interestingly, genes with no currently characterised role in either HSC activation or fibrotic processes were also identified, including CIITA and SERPINB2. Further in silico analysis revealed the prominent signalling pathways downstream of TGF-β1 in LX-2 cells, which will be useful for improving the understanding of how this cytokine influences broader signalling pathways in the activation of HSCs. This work may be of use in the identification of new markers of liver fibrosis and could provide insight into prospective genes or pathways that might be targeted for the amelioration of fibrotic liver disease in the future.

scholarly journals GW501516-activated PPARβ/δ promotes liver fibrosis via p38-JNK MAPK-induced hepatic stellate cell proliferation

2012 ◽  
Vol 2 (1) ◽  
pp. 34 ◽  
Author(s):  
Radina Kostadinova ◽  
Alexandra Montagner ◽  
Erwan Gouranton ◽  
Sébastien Fleury ◽  
Hervé Guillou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Stellate Cell

298 ROLE OF TNF RECEPTORS (TNFR1 AND TNFR2) IN HEPATIC STELLATE CELL PROLIFERATION

2009 ◽  
Vol 50 ◽  
pp. S116
Author(s):  
N. Tarrats ◽  
A. Moles ◽  
J.C. Fernandez-Checa ◽  
M. Marí
Keyword(s):  
Cell Proliferation ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Tnf Receptors
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