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

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

Coagulation Factor V-Major Survival Predictor in Patients of Viral Hepatitis Induced Acute Liver Failure.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3931-3931
Author(s):  
Naveen L. Gupta ◽  
Subhadra Sharma ◽  
Anoop Saraya ◽  
Asok K. Mukhopadhyay
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Viral Hepatitis ◽  
Indian Subcontinent ◽  
Survival Rates ◽  
Coagulation Factor ◽  
Causative Factor ◽  
P Value ◽  
Factor V ◽  
Curative Therapy

Abstract In acute liver failure, variables favoring survival of patients is based on age, interval between onset of jaundice and encephalopathy, coagulation factor level but all these variables were concluded from the studies that were conducted in Western population where etiology most commonly is paracetamol poisoning and metabolic disorders like Wilson’s disease; where as in Indian subcontinent set up major causative factor is viral hepatitis. Thus we exploited the database collected by observational study to investigate major predictors of survival in viral hepatitis induced acute liver failure. Among 40 patients followed for 1 month(7days) or less if died, there were 12 patients who survived. Tha analysis showed that patients who survived had factor V level on day 3 of diagnosis was in the range of 10%–25% and who died had factor V level below 10% (p<0.004). Thus factor V level on day 3 of diagnosis may help in predicting survival in patients of acute liver failure, thus help in triage for the need of orthotopic liver transplantation which is the only definite curative therapy in patients who have poor survival rates. t test outcome No. of patients mean Standard deviation p value standard error of mean group statistics Interval died 26 30.6538 10.8552 <0.002 2.1289 survived 14 6.1429 3.3249 0.8886 FactorV day1 died 26 7.5769 2.8309 >0.05 0.5552 survived 14 12.0000 4.3677 1.1673 Factor VIII day1 died 26 225.3396 156.0354 >0.05 30.6011 survived 14 293.3556 206.3757 55.1562 FactorV day3 died 26 5.9615 2.0096 <0.004 0.3941 survived 14 12.9286 4.8272 1.2901 FactorVIII day3 died 26 248.2509 185.7102 >0.05 36.4208 survived 14 274.7226 206.5798 55.2108 Lactate day1 died 26 74.3308 11.5141 >0.05 2.2581 survived 14 59.0929 8.0789 2.1592 Lactate day3 died 26 78.9500 8.8363 >0.05 1.7329 survived 14 62.5000 9.4086 2.5146 Factor VIII:V day1 died 26 29.8545 16.6385 >0.05 3.2631 survived 14 22.9066 8.9435 2.3902 FActorVIII:V day3 died 26 42.4612 31.8050 <0.003 6.2375 survived 14 20.0944 8.7368 2.3350 pH day1 died 26 7.1365 0.1331 >0.05 2.611E-02 survived 14 7.1443 0.1302 2.648E-02 pH day3 died 26 7.0300 0.1479 >0.05 2.901E-02 survived 14 7.2286 0.1075 2.872E-02 pCO2 day1 died 26 41.8462 7.6036 >0.05 1.4912 survived 14 40.7857 7.5261 2.0114 pCO2 day3 died 26 46.3077 10.3760 >0.05 2.0349 survived 14 43.2857 5.8498 1.5634 pO2 day1 died 26 87.3462 4.3169 >0.05 0.8466 survived 14 86.0000 4.3677 1.1673 pO2 day3 died 26 89.3462 4.0194 >0.05 0.7883 survived 14 89.5000 3.6742 0.9820

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 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 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
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