ArticleThe Journal of clinical investigation2001
Inducible nitric oxide synthase is critical for immune-mediated liver injury in mice.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 196 citations in OpenAlex.
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- Crocetin protects against fulminant hepatic failure induced by lipopolysaccharide/D-galactosamine by decreasing apoptosis, inflammation and oxidative stress in a rat model.Experimental and therapeutic medicine · 2019Article
- mTORC1-mediated polarization of M1 macrophages and their accumulation in the liver correlate with immunopathology in fatal ehrlichiosis.Scientific reports · 2019Article
- Liver disorders related to exposure to gasoline fumes in male rats and role of fenugreek seed supplementation.Environmental science and pollution research international · 2019Article
- Hepatic Lysosomal iNOS Activity Impairs Autophagy in Obesity.Cellular and molecular gastroenterology and hepatology · 2019Article
- The Protective Effect of Sheep Placental Extract on Concanavalin A-induced Liver Injury in Mice.Molecules (Basel, Switzerland) · 2018Article
- Deletion of caveolin-1 attenuates LPS/GalN-induced acute liver injury in mice.Journal of cellular and molecular medicine · 2018Article
- Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2017Article
- Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice.Frontiers in physiology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Concanavalin A (Con A) causes severe TNF-alpha-mediated and IFN-gamma-mediated liver injury in mice. In addition to their other functions, TNF-alpha and IFN-gamma both induce the inducible nitric oxide (NO) synthase (iNOS). Using different models of liver injury, NO was found to either mediate or prevent liver damage. To further elucidate the relevance of NO for liver damage we investigated the role of iNOS-derived NO in the Con A model. We report that iNOS mRNA was induced in livers of Con A-treated mice within 2 hours, with iNOS protein becoming detectable in hepatocytes as well as in Kupffer cells within 4 hours. iNOS-/- mice were protected from liver damage after Con A treatment, as well as in another TNF-alpha-mediated model that is inducible by LPS in D-galactosamine-sensitized (GalN-sensitized) mice. iNOS-deficient mice were not protected after direct administration of recombinant TNF-alpha to GalN-treated mice. Accordingly, pretreatment of wild-type mice with a potent and specific inhibitor of iNOS significantly reduced transaminase release after Con A or GalN/LPS, but not after GalN/TNF-alpha treatment. Furthermore, the amount of plasma TNF-alpha and of intrahepatic TNF-alpha mRNA and protein was significantly reduced in iNOS-/- mice. Our results demonstrate that iNOS-derived NO regulates proinflammatory genes in vivo, thereby contributing to inflammatory liver injury in mice by stimulation of TNF-alpha production.
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