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Cited by 94Cytokine Signaling Pathways and InteractionsLiver physiology and pathologyDrug-Induced Hepatotoxicity and Protection

Lack of gp130 expression in hepatocytes promotes liver injury1 1K.L.S. and T.W. contributed equally to this work.

StreetZ, Konrad L, Wüstefeld, Torsten, Klein, Christian, Kallen, Karl-Josef, Tronche, Francois, Betz, Ullrich A.K, Schütz, Günther, Manns, Michael P +2 more·2003·Gastroenterology
DOI 10.1016/s0016-5085(03)00901-6
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Abstract

Background & aims Interleukin 6 (IL-6) contributes via its signal transducer gp130 to the acute phase response (APR) in hepatocytes. Recent studies indicated that IL-6 is involved in the regulation of different pathophysiologic conditions of the liver. To define the IL-6-dependent intracellular pathways more specifically, we generated a hepatocyte-specific gp130 knockout mouse. Methods Hepatocyte-specific gp130-deficient mice were generated using the Cre-loxP system. Expression of the Cre recombinase was under the control of a hepatocyte-specific control element. Adult mice were challenged with IL-6, oncostatin M (OSM), and LPS. Results Cre expression started at day 10.5 postconception, and a complete deletion of gp130 in hepatocytes was found at day 14 during liver development. The adult liver of these mice showed no abnormalities; however, after IL-6 and OSM stimulation, gp130-dependent pathways (STAT3, APR gene expression) were completely blocked in the liver of these animals. Additionally, challenging hepatocyte-specific gp130 knockout animals with lipopolysaccharides (LPS) lead to an onset of acute liver injury with an increase of hepatocyte apoptosis associated with elevated tumor necrosis factor alpha (TNF-alpha) serum levels and reduced nuclear factor kappaB (NF-kappaB) activation in hepatocytes. Conclusions Our findings demonstrate that gp130 is of minor relevance for embryonal development of hepatocytes. However, the molecule has an essential role in controlling acu…

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Crossref · 10.1016/s0016-5085(03)00901-6

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  • Lack of gp130 expression in hepatocytes renders animals more susceptible to injury during various pathophysiological conditions of the liver.

    “Further experiments in hepatocyte-specific knockout animals showed that lack of gp130 expression in hepatocytes renders these animals more susceptible to injury during various pathophysiological conditions of the liver (25).”

    From The IL-6–gp130–STAT3 pathway in hepatocytes triggers liver protection in T cell–mediated liver injury (2005) · cites this paper as [25]

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Authors
StreetZ, K. L., Wüstefeld, T., Klein, C., Kallen, K.-J., Tronche, F., Betz, U. A. K., Schütz, G., Manns, M. P., Müller, W., & Trautwein, C.
Affiliations
  • Medizinische Hochschule Hannover (DE)
  • Christian-Albrechts-Universität zu Kiel (DE)
  • German Cancer Research Center (DE)
  • Helmholtz Centre for Infection Research (DE)
Corresponding author
Trautwein, Christian
ORCID
Venue
Gastroenterology
Publisher
Elsevier BV
Published
2003-08
Volume
125
Issue
2
Pages
532-543
ISSN
0016-5085 (ISSN-L)
DOI
10.1016/s0016-5085(03)00901-6
OpenAlex
W1516719898
Cited by
94
References
44
Citations by year
2024: 3 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 3 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 5 · 2013: 4 · 2012: 3
FWCI
3.59
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Gastroenterology (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
gp130, interleukin-6, hepatocytes, liver injury, acute phase response, STAT3 signaling, oncostatin M, lipopolysaccharide, hepatocyte-specific knockout, hepatocyte apoptosis, TNF-α, NF-κB
MeSH terms
Animals, DNA-Binding Proteins, Gene Expression Regulation, Lipopolysaccharides, Liver, Male, Membrane Glycoproteins, Tumor Necrosis Factor-alpha, Trans-Activators, Antigens, CD, Interleukin-6, NF-kappa B, Apoptosis, Mice, Knockout, Hepatocytes, STAT3 Transcription Factor, Cytokine Receptor gp130, Mice

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