ArticlePloS one2012
The NF-κB subunit RelA/p65 is dispensable for successful liver regeneration after partial hepatectomy in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Targeting IKKβ Activity to Limit Sterile Inflammation in Acetaminophen-Induced Hepatotoxicity in Mice.Pharmaceutics · 2023Article
- Trans-activation of eotaxin-1 by Brg1 contributes to liver regeneration.Cell death & disease · 2022Article
- Analysis of miRNAs Profiles in Serum of Patients With Steatosis and Steatohepatitis.Frontiers in cell and developmental biology · 2021Article
- Nuclear factor-kappa B influences early phase of compensatory lung growth after pneumonectomy in mice.Journal of biomedical science · 2017Article
- mTOR activation protects liver from ischemia/reperfusion-induced injury through NF-κB pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- A RelA(p65) Thr505 phospho-site mutation reveals an important mechanism regulating NF-κB-dependent liver regeneration and cancer.Oncogene · 2016Article
- A novel comparative pattern count analysis reveals a chronic ethanol-induced dynamic shift in immediate early NF-κB genome-wide promoter binding during liver regeneration.Molecular bioSystems · 2016Article
- Lineage fate of ductular reactions in liver injury and carcinogenesis.The Journal of clinical investigation · 2015Article
- Blockade of the apelin-APJ system promotes mouse liver regeneration by activating Kupffer cells after partial hepatectomy.Journal of gastroenterology · 2015Article
- A novel, dynamic pattern-based analysis of NF-κB binding during the priming phase of liver regeneration reveals switch-like functional regulation of target genes.Frontiers in physiology · 2015Article
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3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transcription factor NF-κB consisting of the subunits RelA/p65 and p50 is known to be quickly activated after partial hepatectomy (PH), the functional relevance of which is still a matter of debate. Current concepts suggest that activation of NF-κB is especially critical in non-parenchymal cells to produce cytokines (TNF, IL-6) to adequately prime hepatocytes to proliferate after PH, while NF-κB within hepatocytes mainly bears cytoprotective functions.
methodsTo study the role of the NF-κB pathway in different liver cell compartments, we generated conditional knockout mice in which the transactivating NF-κB subunit RelA/p65 can be inactivated specifically in hepatocytes (Rela(F/F)AlbCre) or both in hepatocytes plus non-parenchymal cells including Kupffer cells (Rela(F/F)MxCre). 2/3 and 80% PH were performed in controls (Rela(F/F)) and conditional knockout mice (Rela(F/F)AlbCre and Rela(F/F)MxCre) and analyzed for regeneration.
resultsHepatocyte-specific deletion of RelA/p65 in Rela(F/F)AlbCre mice resulted in an accelerated cell cycle progression without altering liver mass regeneration after 2/3 PH. Surprisingly, hepatocyte apoptosis or liver damage were not enhanced in Rela(F/F)AlbCre mice, even when performing 80% PH. The additional inactivation of RelA/p65 in non-parenchymal cells in Rela(F/F)MxCre mice reversed the small proliferative advantage observed after hepatocyte-specific deletion of RelA/p65 so that Rela(F/F)MxCre mice displayed normal cell cycle progression, DNA-synthesis and liver mass regeneration.
conclusionThe NF-κB subunit RelA/p65 fulfills opposite functions in different liver cell compartments in liver regeneration after PH. However, the effects observed after conditional deletion of RelA/p65 are small and do not alter liver mass regeneration after PH. We therefore do not consider RelA/p65-containing canonical NF-κB signalling to be essential for successful liver regeneration after PH.
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