scholarly journals Lymphotoxin-β receptor signaling regulates hepatic stellate cell function and wound healing in a murine model of chronic liver injury

Hepatology ◽  
2008 ◽  
Vol 49 (1) ◽  
pp. 227-239 ◽  
Author(s):  
Richard G. Ruddell ◽  
Belinda Knight ◽  
Janina E. E. Tirnitz-Parker ◽  
Barbara Akhurst ◽  
Lesa Summerville ◽  
...  
Keyword(s):  
Wound Healing ◽  
Liver Injury ◽  
Hepatic Stellate Cell ◽  
Murine Model ◽  
Cell Function ◽  
Stellate Cell ◽  
Chronic Liver ◽  
Receptor Signaling ◽  
Chronic Liver Injury ◽  
Β Receptor

scholarly journals CD248/endosialin critically regulates hepatic stellate cell proliferation during chronic liver injury via a PDGF-regulated mechanism

Gut ◽  
2015 ◽  
Vol 65 (7) ◽  
pp. 1175-1185 ◽  
Author(s):  
Annika Wilhelm ◽  
Victoria Aldridge ◽  
Debashis Haldar ◽  
Amy J Naylor ◽  
Christopher J Weston ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Injury ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Chronic Liver ◽  
Chronic Liver Injury

scholarly journals Hepatic Stellate Cell–Macrophage Crosstalk in Liver Fibrosis and Carcinogenesis

2020 ◽  
Vol 40 (03) ◽  
pp. 307-320
Author(s):  
Michitaka Matsuda ◽  
Ekihiro Seki
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Cell Activation ◽  
Stellate Cell ◽  
Tumor Development ◽  
Mesenchymal Cell ◽  
Chronic Liver ◽  
Health Concern ◽  
Chronic Liver Injury ◽  
Fibrotic Liver

AbstractChronic liver injury due to viral hepatitis, alcohol abuse, and metabolic disorders is a worldwide health concern. Insufficient treatment of chronic liver injury leads to fibrosis, causing liver dysfunction and carcinogenesis. Most cases of hepatocellular carcinoma (HCC) develop in the fibrotic liver. Pathological features of liver fibrosis include extracellular matrix (ECM) accumulation, mesenchymal cell activation, immune deregulation, and angiogenesis, all of which contribute to the precancerous environment, supporting tumor development. Among liver cells, hepatic stellate cells (HSCs) and macrophages play critical roles in fibrosis and HCC. These two cell types interplay and remodel the ECM and immune microenvironment in the fibrotic liver. Once HCC develops, HCC-derived factors influence HSCs and macrophages to switch to protumorigenic cell populations, cancer-associated fibroblasts and tumor-associated macrophages, respectively. This review aims to summarize currently available data on the roles of HSCs and macrophages in liver fibrosis and HCC, with a focus on their interaction.

scholarly journals Relation between liver progenitor cell expansion and extracellular matrix deposition in a CDE-induced murine model of chronic liver injury

Hepatology ◽  
2009 ◽  
Vol 49 (5) ◽  
pp. 1625-1635 ◽  
Author(s):  
Noémi K. M. Van Hul ◽  
Jorge Abarca-Quinones ◽  
Christine Sempoux ◽  
Yves Horsmans ◽  
Isabelle A. Leclercq
Keyword(s):  
Extracellular Matrix ◽  
Liver Injury ◽  
Murine Model ◽  
Cell Expansion ◽  
Progenitor Cell ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Liver Progenitor Cell

Snail1 transcription factor is a critical mediator of hepatic stellate cell activation following hepatic injury

2011 ◽  
Vol 300 (2) ◽  
pp. G316-G326 ◽  
Author(s):  
Melania Scarpa ◽  
Alessia R. Grillo ◽  
Paola Brun ◽  
Veronica Macchi ◽  
Annalisa Stefani ◽  
...  
Keyword(s):  
Wound Healing ◽  
Transcription Factor ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Mrna Expression ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Qrt Pcr

Following liver injury, the wound-healing process is characterized by hepatic stellate cell (HSC) activation from the quiescent fat-storing phenotype to a highly proliferative myofibroblast-like phenotype. Snail1 is a transcription factor best known for its ability to trigger epithelial-mesenchymal transition, to influence mesoderm formation during embryonic development, and to favor cell survival. In this study, we evaluated the expression of Snail1 in experimental and human liver fibrosis and analyzed its role in the HSC transdifferentiation process. Liver samples from patients with liver fibrosis and from mice treated by either carbon tetrachloride (CCl4) or thioacetamide (TAA) were evaluated for mRNA expression of Snail1. The transcription factor expression was investigated by immunostaining and real-time quantitative RT-PCR (qRT-PCR) on in vitro and in vivo activated murine HSC. Snail1 knockdown studies on cultured HSC and on CCl4-treated mice were performed by adenoviral delivery of short-hairpin RNA; activation-related genes were quantitated by real-time qRT-PCR and Western blotting. Snail1 mRNA expression resulted upregulated in murine experimental models of liver injury and in human hepatic fibrosis. In vitro studies showed that Snail1 is expressed by HSC and that its transcription is augmented in in vitro and in vivo activated HSC compared with quiescent HSC. At the protein level, we could observe the nuclear translocation of Snail1 in activated HSC. Snail1 knockdown resulted in the downregulation of activation-related genes both in vitro and in vivo. Our data support a role for Snail1 transcription factor in the hepatic wound-healing response and its involvement in the HSC transdifferentiation process.

Kupffer cell function in chronic liver injury and after partial hepatectomy

1994 ◽  
Vol 194 (1) ◽  
pp. 237-246 ◽  
Author(s):  
Keisuke Hamazaki ◽  
Shizo Sato ◽  
Masayuki Yunoki ◽  
Taku Noda ◽  
Luis Fernando Moreira ◽  
...  
Keyword(s):  
Liver Injury ◽  
Partial Hepatectomy ◽  
Kupffer Cell ◽  
Cell Function ◽  
Chronic Liver ◽  
Chronic Liver Injury

Attenuation of Kupffer Cell Function in Acute on Chronic Liver Injury Enhanced Engraftment of Transplanted Hepatocytes

2007 ◽  
Vol 31 (6) ◽  
pp. 1272-1279 ◽  
Author(s):  
Ray-Hwang Yuan ◽  
Hui-Ling Chen ◽  
Huey-Ling Chen ◽  
Ming-Kung Hsu ◽  
Po-Huang Lee ◽  
...  
Keyword(s):  
Liver Injury ◽  
Kupffer Cell ◽  
Cell Function ◽  
Chronic Liver ◽  
Chronic Liver Injury
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