ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Arachidonic acid stimulates TNFα production in Kupffer cells via a reactive oxygen species-pERK1/2-Egr1-dependent mechanism.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
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- Ablation of secreted phosphoprotein-1 in hepatocytes increases fatty acid oxidation and ameliorates alcohol-associated liver disease.Alcohol, clinical & experimental research · 2024Article
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- A review of nitric oxide and oxidative stress in typical ovulatory women and in the pathogenesis of ovulatory dysfunction in PCOS.Reproductive biology and endocrinology : RB&E · 2023Review
- Role of early growth response 1 in inflammation-associated lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Roles of Gut Microbiota in Alcoholic Liver Disease.International journal of general medicine · 2023Review
- The Integrated "Multiomics" Landscape at Peak Injury and Resolution From Alcohol-Associated Liver Disease.Hepatology communications · 2022Article
- The role of oxidative stress in patients with recurrent pregnancy loss: a review.Reproductive health · 2021Review
- Berberine, A Phytoalkaloid, Inhibits Inflammatory Response Induced by LPS through NF-Kappaβ Pathway: Possible Involvement of the IKKα.Molecules (Basel, Switzerland) · 2021Article
- Translational Approaches with Antioxidant Phytochemicals against Alcohol-Mediated Oxidative Stress, Gut Dysbiosis, Intestinal Barrier Dysfunction, and Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Alteration in the Lipid Profile and the Desaturases Activity in Patients With Severe Pneumonia by SARS-CoV-2.Frontiers in physiology · 2021Article
- Role of RONS and eIFs in Cancer Progression.Oxidative medicine and cellular longevity · 2021Review
- UPLC-MS/MS-Based Rat Serum Metabolomics Reveals the Detoxification Mechanism of Psoraleae Fructus during Salt Processing.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Integrated Strategy FromFrontiers in pharmacology · 2021Article
- Dual RNA-Seq Unveils the Role of the Pseudomonas plecoglossicidaMicroorganisms · 2019Article
- Reactive Oxygen Species: the Dual Role in Physiological and Pathological Conditions of the Human Body.The Eurasian journal of medicine · 2018Review
- Early Growth Response Gene-1 Suppresses Foot-and-Mouth Disease Virus Replication by Enhancing Type I Interferon Pathway Signal Transduction.Frontiers in microbiology · 2018Article
- Participation of Arachidonic Acid Metabolism in the Aortic Aneurysm Formation in Patients with Marfan Syndrome.Frontiers in physiology · 2018Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Kupffer cells are a key source of mediators of alcohol-induced liver damage such as reactive oxygen species, chemokines, growth factors, and eicosanoids. Since diets rich in polyunsaturated fatty acids are a requirement for the development of alcoholic liver disease, we hypothesized that polyunsaturated fatty acids could synergize with ethanol to promote Kupffer cell activation and TNFα production, hence, contributing to liver injury. Primary Kupffer cells from control and from ethanol-fed rats incubated with arachidonic acid showed similar proliferation rates than nontreated cells; however, arachidonic acid induced phenotypic changes, lipid peroxidation, hydroperoxides, and superoxide radical generation. Similar effects occurred in human Kupffer cells. These events were greater in Kupffer cells from ethanol-fed rats, and antioxidants and inhibitors of arachidonic acid metabolism prevented them. Arachidonic acid treatment increased NADPH oxidase activity. Inhibitors of NADPH oxidase and of arachidonic acid metabolism partially prevented the increase in oxidant stress. Upon arachidonic acid stimulation, there was a rapid and sustained increase in TNFα, which was greater in Kupffer cells from ethanol-fed rats than in Kupffer cells from control rats. Arachidonic acid induced ERK1/2 phosphorylation and nuclear translocation of early growth response-1 (Egr1), and ethanol synergized with arachidonic acid to promote this effect. PD98059, a mitogen extracellular kinase 1/2 inhibitor, and curcumin, an Egr1 inhibitor, blocked the arachidonic acid-mediated upregulation of TNFα in Kupffer cells. This study unveils the mechanism whereby arachidonic acid and ethanol increase TNFα production in Kupffer cells, thus contributing to alcoholic liver disease.
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