Proliferation of mouse liver stem/progenitor cells induced by plasma from patients with acute liver failure is modulated by P2Y2 receptor-mediated JNK activation

2013 ◽  
Vol 49 (12) ◽  
pp. 1557-1566 ◽  
Author(s):  
Ting Wang ◽  
Yasuhiro Takikawa ◽  
Asako Watanabe ◽  
Keisuke Kakisaka ◽  
Kanta Oigawa ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Progenitor Cells ◽  
Mouse Liver ◽  
P2y2 Receptor ◽  
Jnk Activation

scholarly journals Erratum to: Proliferation of mouse liver stem/progenitor cells induced by plasma from patients with acute liver failure is modulated by P2Y2 receptor-mediated JNK activation

2014 ◽  
Vol 49 (12) ◽  
pp. 1588-1588
Author(s):  
Ting Wang ◽  
Yasuhiro Takikawa ◽  
Asako Watanabe ◽  
Keisuke Kakisaka ◽  
Kanta Oikawa ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Progenitor Cells ◽  
Mouse Liver ◽  
P2y2 Receptor ◽  
Jnk Activation

scholarly journals Improved Xenogenic Hepatocyte Implantation into Nude Mouse Liver Parenchyma with Acute Liver Failure when Followed by Repeated Anti-Fas Antibody (Jo2) Treatment

2008 ◽  
Vol 17 (5) ◽  
pp. 507-524 ◽  
Author(s):  
Isabelle Vidal ◽  
Nadège Blanchard ◽  
Eliane Alexandre ◽  
Arnaud Gandillet ◽  
Marie-Pierre Chenard-Neu ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Nude Mouse ◽  
Mouse Liver ◽  
Liver Parenchyma

Epiregulin promotes the emergence and proliferation of adult liver progenitor cells

2014 ◽  
Vol 307 (1) ◽  
pp. G50-G57 ◽  
Author(s):  
Kyoko Tomita ◽  
Hiroaki Haga ◽  
Kei Mizuno ◽  
Tomohiro Katsumi ◽  
Chikako Sato ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Liver Regeneration ◽  
Progenitor Cells ◽  
Serum Levels ◽  
Dependent Manner ◽  
Portal Area ◽  
Injury Model

We have previously reported that epiregulin is a growth factor that seems to act on liver progenitor cells (LPCs) during liver regeneration. However, the relationship between epiregulin and LPCs has remained unclear. The aim of the present study was to clarify the role of epiregulin during liver regeneration. The serum levels of epiregulin in patients with acute liver failure were examined. A liver injury model was developed using mice fed a diet containing 0.1% 3.5-diethoxycarbonyl-1.4-dihydrocollidine (DDC) to induce LPCs. We then evaluated the expression of epiregulin and LPCs in these mice. The proliferation of epithelial cell adhesion molecule + LPCs cultured with epiregulin was examined in vitro, and finally epiregulin was overexpressed in mouse liver. In patients with acute liver failure, serum epiregulin levels were elevated significantly. In DDC mice, LPCs emerged around the portal area. Epiregulin was also detected around the portal area during the course of DDC-induced liver injury and was partially coexpressed with Thy1. Serum epiregulin levels in DDC mice were also significantly elevated. Recombinant epiregulin augmented the proliferative capacity of the LPCs in a dose-dependent manner. In mice showing overexpression of epiregulin, the expression of PCNA on hepatocytes was increased significantly. Finally, LPCs emerged around the portal area after epiregulin gene delivery. We concluded that epiregulin promotes the proliferation of LPCs and DNA synthesis by hepatocytes and is upregulated in the serum of patients with liver injury. Furthermore, induction of epiregulin leads to the appearance of LPCs. Epiregulin would be a useful biomarker of liver regeneration.

scholarly journals Follistatin‐controlled activin‐HNF4α‐coagulation factor axis in liver progenitor cells determines outcome of acute liver failure

Hepatology ◽  
2021 ◽  
Author(s):  
Tao Lin ◽  
Shanshan Wang ◽  
Stefan Munker ◽  
Kyounghwa Jung ◽  
Ricardo U. Macías‐Rodríguez ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Progenitor Cells ◽  
Coagulation Factor

scholarly journals Liver Progenitor Cells in Massive Hepatic Necrosis—How Can a Patient Survive Acute Liver Failure?

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 66
Author(s):  
Tao Lin ◽  
Rilu Feng ◽  
Roman Liebe ◽  
Hong-Lei Weng
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Progenitor Cells ◽  
Hepatic Necrosis ◽  
Research Progress ◽  
Pharmacological Management ◽  
Massive Hepatic Necrosis ◽  
New Findings ◽  
Recent Research Progress

Massive hepatic necrosis is the most severe lesion in acute liver failure, yet a portion of patients manage to survive and recover from this high-risk and harsh disease syndrome. The mechanisms underlying recovery remain largely unknown to date. Recent research progress highlights a key role of liver progenitor cells, the smallest biliary cells, in the maintenance of liver homeostasis and thus survival. These stem-like cells rapidly proliferate and take over crucial hepatocyte functions in a severely damaged liver. Hence, the new findings not only add to our understanding of the huge regenerative capability of the liver, but also provide potential new targets for the pharmacological management of acute liver failure in clinical practice.

Effects of Healthy- and Acute Liver Failure Plasma on Differentiated Human Heparg Progenitor Cells in Monolayers and Bioartificial Livers

2016 ◽  
Vol 64 (2) ◽  
pp. S308 ◽  
Author(s):  
M. Van Wenum ◽  
R. Chamuleau ◽  
A. Jongejan ◽  
P. Treskes ◽  
S. Meisner ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Progenitor Cells ◽  
Bioartificial Livers

scholarly journals Noncanonical Wnt5a/JNK Signaling Contributes to the Development of D-Gal/LPS-Induced Acute Liver Failure

2021 ◽  
Author(s):  
Xiang-fen Ji ◽  
Yu-chen Fan ◽  
Fei Sun ◽  
Jing-wei Wang ◽  
kai wang
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Inflammatory Cytokines ◽  
Dependent Manner ◽  
Jnk Signaling ◽  
Wnt5a Expression ◽  
Jnk Activation

Abstract Acute liver failure (ALF) is a deadly clinical disorder with few effective treatments and unclear pathogenesis. In our previous study, we demonstrated that aberrant Wnt5a expression was involved in acute on chronic liver failure. However, the role of Wnt5a in ALF is unknown. We investigated the expression of Wnt5a and its downstream signaling of c-jun N-terminal kinase (JNK) in a mouse model of ALF established by co-injection of D-galactosamine (D-Gal) and lipopolysaccharide (LPS) in C57BL/6 mice. We also investigated the role of Box5, a Wnt5a antagonist in vivo. Moreover, the effect of Wnt5a/JNK signaling on downstream inflammatory cytokines expression, phagocytosis and migration in THP-1 macrophages was studied in vitro. Aberrant Wnt5a expression and JNK activation were detected in D-Gal/LPS-induced ALF mice. Box5 pretreatment reversed JNK activation, and eventually decreased the mortality rate of D-Gal/LPS-treated mice with reduced hepatic necrosis and apoptosis, serum ALT and AST levels, and liver inflammatory cytokines expression, although the last was not significant. We further demonstrated that recombined Wnt5a (rWnt5a) induced tumor necrosis α (TNF-α) and Interleukin-6 (IL-6) mRNA expression, and increased the phagocytosis ability of THP-1 macrophages in a JNK-dependent manner, which could be restored by Box5. In addition, rWnt5a-induced migration of THP-1 macrophages was also turned by Box5. Our findings suggested that Wnt5a/JNK signaling play important role in the development of ALF, and Box5 could have particular hepatoprotecive effects in ALF.

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