ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Hepatocytes produce TNF-α following hypoxia-reoxygenation and liver ischemia-reperfusion in a NADPH oxidase- and c-Src-dependent manner.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
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- Cytoprotective effect of prostacyclin on hepatic ischemia-reperfusion injury.World journal of methodology · 2025Review
- N6-methyladenosine readerWorld journal of gastroenterology · 2025Article
- Enhancing Liver Transplant Outcomes through Liver Precooling to Mitigate Inflammatory Response and Protect Mitochondrial Function.Biomedicines · 2024Article
- Cell-Specific Regulation of Inflammatory Cytokines and Acute-Phase Proteins by the Glucocorticoid Receptor.Mediators of inflammation · 2023Article
- Mild hypothermia ameliorates hepatic ischemia reperfusion injury by inducing RBM3 expression.Apoptosis : an international journal on programmed cell death · 2022Article
- NOX as a Therapeutic Target in Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Ablation of Tumor Necrosis Factor Alpha Receptor 1 Signaling Blunts Steatohepatitis in Peroxisome Proliferator Activated Receptor α-Deficient Mice.Medical research archives · 2022Article
- Effect of Metformin on Myocardial Injury Induced by Hepatic Ischemia-Reperfusion in Rats.Frontiers in pharmacology · 2022Article
- miR-145-5p attenuates inflammatory response and apoptosis in myocardial ischemia-reperfusion injury by inhibiting (NADPH) oxidase homolog 1.Experimental animals · 2021Article
- Hepatic ischemia-reperfusion injury in liver transplant setting: mechanisms and protective strategies.Journal of biomedical research · 2019Article
- A Mitochondrial Specific Antioxidant Reverses Metabolic Dysfunction and Fatty Liver Induced by Maternal Cigarette Smoke in Mice.Nutrients · 2019Article
- Protective role of heme oxygenase-1 in fatty liver ischemia-reperfusion injury.Medical molecular morphology · 2019Review
- PECAM-1 modulates liver damage induced by synergistic effects of TNF-α and irradiation.Journal of cellular and molecular medicine · 2019Article
- Tolerizing CTL by Sustained Hepatic PD-L1 Expression Provides a New Therapy Approach in Mouse Sepsis.Theranostics · 2019Article
- Loss of PDK4 switches the hepatic NF-κB/TNF pathway from pro-survival to pro-apoptosis.Hepatology (Baltimore, Md.) · 2018Article
- nox2/cybb Deficiency Affects Zebrafish Retinotectal Connectivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function.International journal of molecular sciences · 2018Review
- Pre-conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion.Journal of cellular and molecular medicine · 2017Review
- Sirtuin 2 aggravates postischemic liver injury by deacetylating mitogen-activated protein kinase phosphatase-1.Hepatology (Baltimore, Md.) · 2017Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cell line studies have previously demonstrated that hypoxia-reoxygenation (H/R) leads to the production of NADPH oxidase 1 and 2 (NOX1 and NOX2)-dependent reactive oxygen species (ROS) required for the activation of c-Src and NF-κB. We now extend these studies into mouse models to evaluate the contribution of hepatocytes to the NOX- and c-Src-dependent TNF-α production that follows H/R in primary hepatocytes and liver ischemia-reperfusion (I/R). In vitro, c-Src-deficient primary hepatocytes produced less ROS and TNF-α following H/R compared with controls. In vivo, c-Src-KO mice also had impaired TNF-α and NF-κB responses following partial lobar liver I/R. Studies in NOX1 and p47phox knockout primary hepatocytes demonstrated that both NOX1 and p47phox are partially required for H/R-mediated TNF-α production. To further investigate the involvement of NADPH oxidases in the production of TNF-α following liver I/R, we performed additional in vivo experiments in knockout mice deficient for NOX1, NOX2, p47phox, Rac1, and/or Rac2. Cumulatively, these results demonstrate that NOX2 and its activator subunits (p47phox and Rac) control the secretion of TNF-α by the liver following I/R. Interestingly, in the absence of Kupffer cells and NOX2, NOX1 played a dominant role in TNF-α production following hepatic I/R. However, NOX1 deletion alone had little effect on I/R-induced TNF-α. Thus Kupffer cell-derived factors and NOX2 act to suppress hepatic NOX1-dependent TNF-α production. We conclude that c-Src and NADPH oxidase components are necessary for redox-mediated production of TNF-α following liver I/R and that hepatocytes play an important role in this process.
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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.