scholarly journals PHYSIOLOGICAL FACTORS AND LIVER CELL FUNCTION

1959 ◽  
Vol 7 (4) ◽  
pp. 235-236 ◽  
Author(s):  
LEON L. MILLER
Keyword(s):  
Liver Cell ◽  
Cell Function ◽  
Physiological Factors

Liver cell hydration and integrin signaling

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Michele Bonus ◽  
Dieter Häussinger ◽  
Holger Gohlke
Keyword(s):  
Cell Volume ◽  
Liver Cell ◽  
Cell Function ◽  
The Other ◽  
Signaling Cascades ◽  
Integrin Signaling ◽  
Volume Changes ◽  
The One ◽  
And Oxidative Stress

Abstract Liver cell hydration (cell volume) is dynamic and can change within minutes under the influence of hormones, nutrients, and oxidative stress. Such volume changes were identified as a novel and important modulator of cell function. It provides an early example for the interaction between a physical parameter (cell volume) on the one hand and metabolism, transport, and gene expression on the other. Such events involve mechanotransduction (osmosensing) which triggers signaling cascades towards liver function (osmosignaling). This article reviews our own work on this topic with emphasis on the role of β1 integrins as (osmo-)mechanosensors in the liver, but also on their role in bile acid signaling.

Liver Cell Hydration and Cell Function

2010 ◽  
pp. 137-140
Author(s):  
Dieter Häussinger
Keyword(s):  
Liver Cell ◽  
Cell Function

Interactions Between Liver Cell Volume and Liver Cell Function

1992 ◽  
pp. 413-432
Author(s):  
Dieter Häussinger ◽  
Florian Lang
Keyword(s):  
Cell Volume ◽  
Liver Cell ◽  
Cell Function

Complement and liver cell function in 53 patients with liver disease

1973 ◽  
Vol 55 (6) ◽  
pp. 783-790 ◽  
Author(s):  
Olivier Kourilsky ◽  
Colette Leroy ◽  
AndréP. Peltier
Keyword(s):  
Liver Disease ◽  
Liver Cell ◽  
Cell Function

Control of liver cell function by the hydration state

1994 ◽  
Vol 22 (2) ◽  
pp. 497-502 ◽  
Author(s):  
Dieter Häussinger ◽  
William Newsome ◽  
Stephan vom Dahl ◽  
Barbara Stoll ◽  
Birgitta Noe ◽  
...  
Keyword(s):  
Liver Cell ◽  
Cell Function ◽  
Hydration State

scholarly journals Conditioned media of Kupffer and endothelial liver cells influence protein phosphorylation in parenchymal liver cells. Involvement of prostaglandins

1988 ◽  
Vol 252 (2) ◽  
pp. 601-605 ◽  
Author(s):  
E Casteleijn ◽  
J Kuiper ◽  
H C Van Rooij ◽  
J F Koster ◽  
T J Van Berkel
Keyword(s):  
Protein Phosphorylation ◽  
Liver Cell ◽  
Cell Function ◽  
Liver Cells ◽  
Conditioned Media ◽  
Prostaglandin D2 ◽  
Phosphorylation State ◽  
Glucose Homoeostasis ◽  
Parenchymal Liver ◽  
Parenchymal Cells

The possible role of Kupffer and endothelial liver cells in the regulation of parenchymal-liver-cell function was assessed by studying the influence of conditioned media of isolated Kupffer and endothelial cells on protein phosphorylation in isolated parenchymal cells. The phosphorylation state of three proteins was selectively influenced by the conditioned media. The phosphorylation state of an Mr-63,000 protein was decreased and the phosphorylation state of an Mr-47,000 and an Mr-97,000 protein was enhanced by these media. These effects could be mimicked by adding either prostaglandin E1, E2 or D2. Both conditioned media and prostaglandins stimulated the phosphorylase activity in parenchymal liver cells, suggesting that the Mr-97,000 phosphoprotein might be phosphorylase. Parenchymal liver cells secrete a phosphoprotein of Mr-63,000 and pI 5.0-5.5. The phosphorylation of this protein is inhibited by Kupffer- and endothelial-liver-cell media, and prostaglandins E1, E2 and D2 had a similar effect. The data indicate that Kupffer and endothelial liver cells secrete factors which influence the protein phosphorylation in parenchymal liver cells. This forms further evidence that products from non-parenchymal liver cells, in particular prostaglandin D2, might regulate glucose homoeostasis and/or other specific metabolic processes inside parenchymal cells. This stresses the concept of cellular communication inside the liver as a way by which the liver can rapidly respond to extrahepatic signals.

scholarly journals Human fetuin/α2HS-glycoprotein level as a novel indicator of liver cell function and short-term mortality in patients with liver cirrhosis and liver cancer

2002 ◽  
Vol 14 (4) ◽  
pp. 389-394 ◽  
Author(s):  
László Kalabay ◽  
Lajos Jakab ◽  
Zoltán Prohászka ◽  
George Füst ◽  
Zsuzsa Benkö ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Cancer ◽  
Liver Cell ◽  
Cell Function ◽  
Short Term ◽  
Short Term Mortality

scholarly journals Procalcitonin Impairs Liver Cell Viability and Function In Vitro: A Potential New Mechanism of Liver Dysfunction and Failure during Sepsis?

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Martin Sauer ◽  
Sandra Doß ◽  
Johannes Ehler ◽  
Thomas Mencke ◽  
Nana-Maria Wagner
Keyword(s):  
Metabolic Activity ◽  
Liver Cell ◽  
Liver Dysfunction ◽  
Cell Function ◽  
Positive Control ◽  
Novel Approach ◽  
Biosensor System ◽  
Cellular Integrity ◽  
And Function

Purpose. Liver dysfunction and failure are severe complications of sepsis and result in poor outcome and increased mortality. The underlying pathologic mechanisms of hepatocyte dysfunction and necrosis during sepsis are only incompletely understood. Here, we investigated whether procalcitonin, a biomarker of sepsis, modulates liver cell function and viability.Materials and Methods. Employing a previously characterized and patented biosensor system evaluating hepatocyte toxicity in vitro, human hepatocellular carcinoma cells (HepG2/C3A) were exposed to 0.01–50 ng/mL procalcitonin for2×72 h and evaluated for proliferation, necrosis, metabolic activity, cellular integrity, microalbumin synthesis, and detoxification capacity. Acetaminophen served as positive control. For further standardization, procalcitonin effects were confirmed in a cellular toxicology assay panel employing L929 fibroblasts. Data were analyzed using ANOVA/Tukey’s test.Results. Already at concentrations as low as 0.25 ng/mL, procalcitonin induced HepG2/C3A necrosis (P<0.05) and reduced metabolic activity, cellular integrity, synthesis, and detoxification capacity (allP<0.001). Comparable effects were obtained employing L929 fibroblasts.Conclusion. We provide evidence for procalcitonin to directly impair function and viability of human hepatocytes and exert general cytotoxicity in vitro.Therapeutical targeting of procalcitonin could thus display a novel approach to reduce incidence of liver dysfunction and failure during sepsis and lower morbidity and mortality of septic patients.

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