ArticleToxicology and applied pharmacology2014
Analysis of changes in hepatic gene expression in a murine model of tolerance to acetaminophen hepatotoxicity (autoprotection).
Article in Toxicology and applied pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Evaluation of the Feasibility of In Vitro Metabolic Interruption of Trimethylamine with Resveratrol Butyrate Esters and Its Purified Monomers.Molecules (Basel, Switzerland) · 2024Article
- Single-cell RNA sequencing reveals the dynamics of hepatic non-parenchymal cells in autoprotection against acetaminophen-induced hepatotoxicity.Journal of pharmaceutical analysis · 2023Article
- Changes of urine metabolite profiles are induced by inactivated influenza vaccine inoculations in mice.Scientific reports · 2019Article
- Vanin 1: Its Physiological Function and Role in Diseases.International journal of molecular sciences · 2019Review
- Unsupervised identification of disease states from high-dimensional physiological and histopathological profiles.Molecular systems biology · 2019Article
- Integrated analysis of microRNA and mRNA expression profiles highlights the complex and dynamic behavior of toosendanin-induced liver injury in mice.Scientific reports · 2016Article
- Oxidative stress-responsive transcription factor NRF2 is not indispensable for the human hepatic Flavin-containing monooxygenase-3 (FMO3) gene expression in HepG2 cells.Toxicology in vitro : an international journal published in association with BIBRA · 2016Article
- From hepatoprotection models to new therapeutic modalities for treating liver diseases: a personal perspective.F1000Research · 2016Review
- Adaptation to acetaminophen exposure elicits major changes in expression and distribution of the hepatic proteome.Scientific reports · 2015Article
- Differential Fmo3 gene expression in various liver injury models involving hepatic oxidative stress in mice.Toxicology · 2014Article
- Role of Nrf2 in chronic liver disease.World journal of gastroenterology · 2014Review
- Tolerance to acetaminophen hepatotoxicity in the mouse model of autoprotection is associated with induction of flavin-containing monooxygenase-3 (FMO3) in hepatocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Pretreatment of mice with a low hepatotoxic dose of acetaminophen (APAP) results in resistance to a subsequent, higher dose of APAP. This mouse model, termed APAP autoprotection was used here to identify differentially expressed genes and cellular pathways that could contribute to this development of resistance to hepatotoxicity. Male C57BL/6J mice were pretreated with APAP (400mg/kg) and then challenged 48h later with 600mg APAP/kg. Livers were obtained 4 or 24h later and total hepatic RNA was isolated and hybridized to Affymetrix Mouse Genome MU430_2 GeneChip. Statistically significant genes were determined and gene expression changes were also interrogated using the Causal Reasoning Engine (CRE). Extensive literature review narrowed our focus to methionine adenosyl transferase-1 alpha (MAT1A), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), flavin-containing monooxygenase 3 (Fmo3) and galectin-3 (Lgals3). Down-regulation of MAT1A could lead to decreases in S-adenosylmethionine (SAMe), which is known to protect against APAP toxicity. Nrf2 activation is expected to play a role in protective adaptation. Up-regulation of Lgals3, one of the genes supporting the Nrf2 hypothesis, can lead to suppression of apoptosis and reduced mitochondrial dysfunction. Fmo3 induction suggests the involvement of an enzyme not known to metabolize APAP in the development of tolerance to APAP toxicity. Subsequent quantitative RT-PCR and immunochemical analysis confirmed the differential expression of some of these genes in the APAP autoprotection model. In conclusion, our genomics strategy identified cellular pathways that might further explain the molecular basis for APAP autoprotection.
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