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Gene expression data from THP-1 cells exposed to exosomes from acetaminophen-treated or vehicle-treated hepatocytes or corresponding mock- or medium-controls

ABSTRACT: In the present study we examined the effect of hepatocyte-derived exosomes (HDE) on innate immune cells by treating a human monocyte cell line (THP-1 cells) with exosomes collected from the culture medium of acetaminophen (APAP)-treated and untreated primary human hepatocytes and comparing the cytokine response to THP-1 cells treated with mock- and medium-controls. We profiled the gene expression changes observed in the HDE-exposed monocytes prior to LPS stimulation. Findings from our research suggest that HDE may be essential for maintaining immune homeostasis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE125690 | GEO | 2019/12/31

REPOSITORIES: GEO

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Gene expression data from THP-1 cells exposed to exosomes from acetaminophen-treated or vehicle-treated hepatocytes or corresponding mock- or medium-controls

Project description:Gene expression data from THP-1 cells exposed to exosomes from acetaminophen-treated or vehicle-treated hepatocytes or corresponding mock- or medium-controls

| PRJNA517174 | ENA

Next-gen sequencing for miRNA content of exosomes and hepatocytes in mice with acetaminophen toxicity

Project description:Micro RNA content of extracellular vesicles/exosomes may serve as a marker of certain pathophysiological conditions. We report differential expression of micro RNA in exosomes isolated from mouse blood or medium of cultured primary mouse hepatocytes versus parental hepatocytes or whole liver. Studies included exosomes from blood of mice or medium of cultured primary hepatocytes with acetaminophen toxicity as well as a potentially therapeutic cytokine with acetaminophen.

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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

2008-06-14 | E-GEOD-5652 | biostudies-arrayexpress

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. For the toxicogenomics study, samples were as followed: five mice per low, medium, and high dose group at 1 day, and five mice in the high dose group at 2 days. One set of vehicle controls (n=5) per day was used. The total number of samples was 70.

2014-12-16 | E-GEOD-51969 | biostudies-arrayexpress

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

2013-06-08 | GSE37874 | GEO

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

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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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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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

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

Project description:Genetic disruption of thioredoxin reductase 1 protects against acetaminophen (APAP) toxicity. To determine the role of the thioredoxin system on xenobiotic metabolism we challeneged wildtype and txnrd1liver-null mice with acetaminophen. Adult male wildtype and txnrd1 liver-null mice (C57BL6/J) were treated with either saline (PBS) or 100mg/kg APAP. Liver RNA was harvested eight hours after challenge and processed for microarray analysis. Comparison of 2 treatment conditions in 2 genotypes, biological replicates in triplicate.

2013-06-08 | E-GEOD-37874 | biostudies-arrayexpress

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