IKKβ Is Required for Prevention of Apoptosis Mediated by Cell-Bound but Not by Circulating TNFα
Open accessAbstract
IkappaB kinase beta (IKKbeta) is required for NF-kappaB activation and suppression of TNFalpha-mediated liver apoptosis. To investigate how IKKbeta suppresses apoptosis, we generated hepatocyte-specific Ikkbeta knockout mice, Ikkbeta(Deltahep), which exhibit little residual NF- kappaB activity but are healthy with normal liver function. Unexpectedly, Ikkbeta(Deltahep) mice are slightly more sensitive than controls to LPS-induced liver apoptosis but are highly susceptible to liver destruction following concanavalin A (ConA)-induced T cell activation. Unlike LPS, a potent inducer of circulating TNFalpha, ConA exerts cytotoxic effects through cell-bound TNFalpha, which activates type 1 and 2 TNF receptors (TNFR). While TNFR2 does not contribute to NF-kappaB activation, it is important for ConA-induced JNK activation, which is augmented by the absence of IKKbeta. Using JNK-deficient mice we show that JNK is required for ConA-induced liver damage. Thus, the antiapoptotic function of IKKbeta, which is most critical in situations that involve cell-bound TNFalpha, is mediated partially through attenuation of JNK activity.
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When NFκB function is selectively inactivated in hepatocytes, IL-6 mRNA production is severely muted in whole livers obtained from mice at 4 h after injection of LPS.
“Maeda et al. established that when NFκB function is selectively inactivated in hepatocytes, IL-6 mRNA production is severely muted in whole livers obtained from mice at 4 h after injection of LPS [6].”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
NFκB can act upstream of IL-6 to control synthesis.
“and as NFκB can act upstream of IL-6 to control synthesis [6], [7]”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
IL-6 mRNA production occurs under the transcriptional control of NFκB.
“IL-6 mRNA production is known to subsequently occur under the transcriptional control of NFκB [6], [7].”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
The rapid time frame and hepatocyte-specific NFκB defect in Maeda et al. suggested that hepatocytes might also serve as a direct source of IL-6 during an acute phase reaction.
“As the time frame in which the observed the changes in IL-6 was rapid, and the induced NFκB defect was hepatocyte-specific, these experiments suggested to us that hepatocytes, in addition to immune cells, might also serve as a direct source of IL-6 during an acute phase reaction, i.e. the hepatic response might also have an autocrine component.”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
The p65 data supports the finding of a paucity of nuclear NFκB in hepatocyte-specific NFκB knockouts at 1 h after LPS injection.
“Our p65 data supports the finding that there was a paucity of nuclear NFκB reported by Maeda et al when nuclei from hepatocyte-specific NFκB knockouts, versus their control counterparts, were subjected to EMSA at 1 h following LPS injection [6]”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
The two other studies that found NFκB elevated in liver at 1 h post-LPS used gel shift analyses without subsequent supershift confirmation.
“the other two investigations were performed using gel shift analyses without subsequent supershift confirmation to ensure that both subunits of prototypical NFκB were in the DNA-binding complex.”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [6]
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Self-citation
- Authors
- Maeda, S., Chang, L., Li, Z.-W., Luo, J.-L., Leffert, H., & Karin, M.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Karin, Michael
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2003-11
- Volume
- 19
- Issue
- 5
- Pages
- 725-737
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2057942179
- Cited by
- 286
- References
- 65
- Citations by year
- 2024: 3 · 2023: 3 · 2022: 4 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 11 · 2016: 12 · 2015: 9 · 2014: 9 · 2013: 12 · 2012: 16
- FWCI
- 8.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI 43477)
- National Institute of Environmental Health Sciences (P42ES010337, ES10337, ES 06376, R01ES006376)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- IκB kinase β, NF-κB activation, apoptosis, TNF receptor 2, JNK, concanavalin A, T cell activation, liver injury, hepatocyte-specific knockout mice, antiapoptotic function
- MeSH terms
- Animals, Concanavalin A, Lipopolysaccharides, Liver, Mice, Inbred C57BL, T-Lymphocytes, Tumor Necrosis Factor-alpha, Antigens, CD, Apoptosis, Protein Serine-Threonine Kinases, Receptors, Tumor Necrosis Factor, Mice, Knockout, Mitogen-Activated Protein Kinases, Receptors, Tumor Necrosis Factor, Type II, JNK Mitogen-Activated Protein Kinases, Mice, I-kappa B Kinase
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