ArticleJournal of cellular physiology2012
Hepatocyte growth factor preferentially activates the anti-inflammatory arm of NF-κB signaling to induce A20 and protect renal proximal tubular epithelial cells from inflammation.
Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Anti-inflammatory Prowess of endothelial progenitor cells in the realm of biology and medicine.NPJ Regenerative medicine · 2024Review
- ZnT8 Exerts Anti-apoptosis of Kidney Tubular Epithelial Cell in Diabetic Kidney Disease Through TNFAIP3-NF-κB Signal Pathways.Biological trace element research · 2023Article
- Epidermal growth factor upregulates the expression of A20 in hepatic cells via the MEK1/MSK1/p-p65 (Ser276) signaling pathway.American journal of translational research · 2021Article
- Dexmedetomidine Preconditioning Protects Rats from Renal Ischemia-Reperfusion Injury Accompanied with Biphasic Changes of Nuclear Factor-Kappa B Signaling.Journal of immunology research · 2020Article
- Clinical assessment and pathophysiology ofThe journal of venomous animals and toxins including tropical diseases · 2020Article
- Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine.Mediators of inflammation · 2020Review
- A20 rescues hepatocytes from apoptosis through the NF-κB signaling pathway in rats with acute liver failure.Bioscience reports · 2019Article
- Calcitriol Ameliorates AngiotensinII-Induced Renal Injury Partly via Upregulating A20.Inflammation · 2017Article
- Antimicrobial Peptide Epinecidin-1 Modulates MyD88 Protein Levels via the Proteasome Degradation Pathway.Marine drugs · 2017Article
- Late intervention with the small molecule BB3 mitigates postischemic kidney injury.American journal of physiology. Renal physiology · 2016Article
- Hypothermic machine perfusion increases A20 expression which protects renal cells against ischemia/reperfusion injury by suppressing inflammation, apoptosis and necroptosis.International journal of molecular medicine · 2016Article
- Induction of the inflammatory regulator A20 by gibberellic acid in airway epithelial cells.British journal of pharmacology · 2016Article
- Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis.Nature reviews. Nephrology · 2015Review
- Adenovirus-mediated dual gene expression of human interleukin-10 and hepatic growth factor exerts protective effect against CCl4-induced hepatocyte injury in rats.Digestive diseases and sciences · 2012Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation induces the NF-κB dependent protein A20 in human renal proximal tubular epithelial cells (RPTEC), which secondarily contains inflammation by shutting down NF-κB activation. We surmised that inducing A20 without engaging the pro-inflammatory arm of NF-κB could improve outcomes in kidney disease. We showed that hepatocyte growth factor (HGF) increases A20 mRNA and protein levels in RPTEC without causing inflammation. Upregulation of A20 by HGF was NF-κB/RelA dependent as it was abolished by overexpressing IκBα or silencing p65/RelA. Unlike TNFα, HGF caused minimal IκBα and p65/RelA phosphorylation, with moderate IκBα degradation. Upstream, HGF led to robust and sustained AKT activation, which was required for p65 phosphorylation and A20 upregulation. While HGF treatment of RPTEC significantly increased A20 mRNA, it failed to induce NF-κB dependent, pro-inflammatory MCP-1, VCAM-1, and ICAM-1 mRNA. This indicates that HGF preferentially upregulates protective (A20) over pro-inflammatory NF-κB dependent genes. Upregulation of A20 supported the anti-inflammatory effects of HGF in RPTEC. HGF pretreatment significantly attenuated TNFα-mediated increase of ICAM-1, a finding partially reversed by silencing A20. In conclusion, this is the first demonstration that HGF activates an AKT-p65/RelA pathway to preferentially induce A20 but not inflammatory molecules. This could be highly desirable in acute and chronic renal injury where A20-based anti-inflammatory therapies are beneficial.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.