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Modulation of the transcriptional response to recombinant IFN-β by Acetaminophen

ABSTRACT: We examined the effect of acetaminophen (APAP) on the transcriptional response induced by interferon-β (IFN-β). Transcript levels from total RNA isolated rom murine livers were determined using G4121B whole genome arrays. Keywords: Pharmakinetics, drug treatment

ORGANISM(S): Mus musculus

PROVIDER: GSE18949 | GEO | 2010/10/18

SECONDARY ACCESSION(S): PRJNA120983

REPOSITORIES: GEO

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Modulation of the transcriptional response to recombinant IFN-Î² by Acetaminophen

Project description:We examined the effect of acetaminophen (APAP) on the transcriptional response induced by interferon-Î² (IFN-Î²). Transcript levels from total RNA isolated rom murine livers were determined using G4121B whole genome arrays. Keywords: Pharmakinetics, drug treatment 6-8 week male CD-1 mice were administered vehicle alone, APAP, IFN-Î² or IFN-Î² + APAP (n=5 per treatment per time point 40 animals total) and were euthanized at 1.5 or 4 hours post-treatment. Agilent 22k whole genome arrays were used to measure changes in mRNA transcripts in the liver mRNA. Stratatagene Universal Mouse RNA was used as a reference.

2010-10-18 | E-GEOD-18949 | biostudies-arrayexpress

Transcription profiling of rat blood and liver exposed to acetaminophen (APAP)

Project description:This SuperSeries is composed of the following subset Series:; GSE5593: Acetaminophen (APAP) Rat Blood Training Gene Expression Data Set; GSE5594: Acetaminophen (APAP) Rat Blood Test Gene Expression Data Set; GSE5595: Acetaminophen (APAP) Rat Liver Test Gene Expression Data Set; The Supplementary files (appended below) contain the mapping for the decoding of blinded samples. Experiment Overall Design: Refer to individual Series

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Protein Targets of Acetaminophen Covalent Binding in Rat and Mouse Liver Studied by LC-MS/MS

Project description:Acetaminophen (N-acetyl-p-aminophenol; APAP) is a mild analgesic and antipyretic used commonly worldwide. Although APAP is considered a safe and effective over-the-counter medication, it is also the leading cause of drug-induced acute liver failure. Its hepatotoxicity has been linked to the covalent binding of its reactive metabolite, N-acetyl p-benzoquinone imine (NAPQI), to proteins. The aim of this in vivo study was to identify APAP-protein targets in both rat and mouse liver, and to compare the results from both species, using bottom-up proteomics and targeted multiple reaction monitoring (MRM) experiments. Livers from rats and mice, treated with APAP, were homogenized and digested by trypsin. Digests were then fractionated by mixed-mode solid-phase extraction prior to liquid chromatography-tandem mass spectrometry (LC-MS/MS) using scheduled multiple reaction monitoring (MRM) acquisition. The targeted assays were optimized based on high-resolution MS/MS data from information-dependent acquisition (IDA) using control liver homogenates treated with a custom alkylating reagent forming a positional isomer of the APAP modification on all cysteine residues, in order to build an in-house modified peptide database for targeted analysis. A list of putative in vivo targets of APAP were screened from previous in vitro studies, data-dependent high-resolution MS/MS analyses of liver digests, as well as selected proteins from the target protein database (TPDB), an online resource which references previous reports of proteins found to be modified by acetaminophen. Multiple protein targets of APAP in each species were found, while confirming modification sites.

2022-02-17 | PXD027674 | Pride

Gene expression profiles of acetaminophen, isoniazid, and paraquat treated C57BL/6 mice

Project description:Toxicogenomics (tgx) is used as a tool to identify mechanisms and markers of necrosis in C57BL/6 mice treated by oral gavage using acetaminophen (APAP), isoniazid (INZ), and paraquat (PQ). Critical doses for tgx analysis were derived from a 25 day dose range finding study. For tgx analysis, livers of mice were collected 1 and 2 days after a single compound dose of 168.75, 225, and 300 mg/kg bw for APAP; 12.5, 25, and 50 mg/kg bw for PQ; and 22, 44, and 88 mg/kg bw for INZ. All samples were diluted in water.

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Shifted Metabolic Bias in Livers of Mice Lacking Hepatocytic Thioredoxin Reductase-1 Protects Against Acetaminophen Toxicity

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Role of YAP in Liver Regeneration After Acetaminophen Overdose

Project description:Overdose of acetaminophen (APAP) is the major cause of acute liver failure in the Western world with very limited treatment options. Previous studies from our groups and others have shown that timely activation of liver regeneration is a critical determinant of transplant-free survival of APAP-induced acute liver failure (ALF) patients. We used affy microarrays to explore the mechanisms of transcriptional expression in YAP-KO mice after 300mg/kg APAP overdose.

2021-10-04 | GSE183119 | GEO

Differential Regulation of Mitogen-Activated Protein Kinases by Acetaminophen in TAMH cells

Project description:Acetaminophen (APAP), a widely used analgesic and antipyretic that is considered to be relatively safe at recommended doses, is the leading cause of drug-induced liver failure in the United States. 3M-bM-^@M-^Y-Hydroxyacetanilide (AMAP), a regioisomer of acetaminophen is useful as a comparative tool for studying APAP-induced toxicity since it is non-toxic relative to APAP. TGF-alpha transgenic mouse hepatocytes were treated with both isomers to investigate mitogen-activated protein kinase cascades in order to differentiate their toxicological outcomes. Mitogen-activated protein kinase (MAPK) cascade expression and activation were measured using microarray and Bioplex technologies, respectively. APAP treatment led to c-Jun N-terminal kinase (JNK) activation, whereas AMAP treatment led to the activation of extracellular-signal-regulated protein kinase (ERK). The microarray data suggested APAP treatment may upregulate gene expression at multiple levels of the JNK cascade including a JNK-related scaffold protein. Expression data was related to phosphoprotein levels using the Bioplex system. APAP treatment led to a significant activation of JNK compared to its regioisomer. In contrast, microarray analysis of AMAP showed a slight upregulation of ERK gene activity. Furthermore, Bioplex data showed AMAP treatment led to significant ERK phosphorylation compared to APAP. Cell viability assays confirmed that APAP-induced activation of JNK was related to higher rates of cell death, whereas activation of ERK by AMAP may be cytoprotective. 27 arrays, 9 experimental groups, 2hr AMAP, 2hr APAP, 2hr Control, 6hr AMAP, 6hr APAP, 6hr Control, 24hr AMAP, 24hr APAP, 24hr Control.

2010-07-06 | E-GEOD-18614 | biostudies-arrayexpress

Investigating the effect of inflammatory conditions on acetaminophen-induced liver injury using 3D human multicellular microtissues

Project description:To investigate the molecular mechanisms of the inflammation-mediated exacerbation of increased acetaminophen (APAP) toxicity.

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Shifted Metabolic Bias in Livers of Mice Lacking Hepatocytic Thioredoxin Reductase-1 Protects Against Acetaminophen Toxicity

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Expression data from mouse liver after Acetaminophen intoxication

Project description:Acetaminophen (APAP) is the most widely used analgesic in the United States. Its acute overdose causes liver damage by inducing localized centrilobular cell death. Because of widespread use, APAP toxicity has become the most frequent cause of acute liver failure. Many factors have been associated with the susceptibility of APAP-induced liver injuries, however, few of them have been confirmed and used in the clinical setting. We tried to identify the subset of factors that could affect susceptibility to APAP-induced liver injury by an integrative genetic, transcriptional and 2-D-NMR-based metabolomic analysis across a panel of inbred mouse strains.

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