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Affect of liver transcriptome by acute acetaminophen exposure [miRNA]

ABSTRACT: To study the global changes of liver transcriptome after acetaminophen overdose.

ORGANISM(S): Merkel cell polyomavirus Rattus norvegicus Mus musculus Human gammaherpesvirus 8 JC polyomavirus Betapolyomavirus macacae Homo sapiens Murid gammaherpesvirus 4 Human immunodeficiency virus 1 Human betaherpesvirus 5 Human alphaherpesvirus 2 Human alphaherpesvirus 1 Betapolyomavirus hominis human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE42181 | GEO | 2013/05/03

SECONDARY ACCESSION(S): PRJNA179241

REPOSITORIES: GEO

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Affect of liver transcriptome by acute acetaminophen exposure [miRNA]

Project description:To study the global changes of liver transcriptome after acetaminophen overdose. To study the global changes of transcriptome in the liver after acetaminophen overdose. Eight week old female C57BL/6 mice were fasted for 24 hours prior to a single intraperitoneal injection of 350mg/kg of acetaminophen in phosphate buffer saline (PBS) (treatment group) or PBS (control group). The mice were euthanized at different time points post exposure; plasma and tissue samples were collected for pathological examination and biochemical analyses.

2013-05-03 | E-GEOD-42181 | biostudies-arrayexpress

Affect of liver transcriptome by acute acetaminophen exposure [mRNA]

Project description:To study the global changes of liver transcriptome after acetaminophen overdose.

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Affect of liver transcriptome by acute acetaminophen exposure [mRNA]

2013-05-03 | E-GEOD-42178 | biostudies-arrayexpress

Novel Protective Role of Nicotinamide Phosphoribosyltransferase in Acetaminophen-induced Acute Liver Injury in Mice

Project description:Acetaminophen overdose is the most common cause of acute liver injury (ALI) or acute liver failure in the USA. Its pathogenetic mechanisms are incompletely understood. Additional studies are warranted to identify new genetic risk factors for more mechanistic insights and new therapeutic target discoveries. The objective of this study was to explore the role and mechanisms of nicotinamide phosphoribosyltransferase (NAMPT) in acetaminophen-induced ALI. C57BL/6 Nampt gene wild type (Nampt+/+)-, heterozygous knockout (Nampt+/-)-, and overexpression (NamptOE)-mice were treated with overdose of acetaminophen, followed by histological, biochemical, and transcriptomic evaluation of liver injury. The mechanism of Nampt in acetaminophen -induced hepatocytic toxicity was also explored in cultured primary hepatocytes. Three lines of evidence have convergently demonstrated that acetaminophen overdose triggers the most severe oxidative stress and necrosis, and the highest expression of key necrosis driving genes in Nampt+/- mice, while the effects in NamptOE mice were least severe relative to Nampt+/+ mice. These findings support that NAMPT protects against acetaminophen induced ALI.

2018-04-03 | GSE110787 | 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

Role of YAP in Liver Regeneration After Acetaminophen Overdose

Project description:Role of YAP in Liver Regeneration After Acetaminophen Overdose

| PRJNA759224 | ENA

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.

2009-08-14 | GSE17649 | GEO

Affect of liver transcriptome by acute acetaminophen exposure

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-05-03 | GSE42182 | GEO

Affect of liver transcriptome by acute acetaminophen exposure

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-05-03 | E-GEOD-42182 | biostudies-arrayexpress

Cryopreserved human alternatively activated macrophages promote resolution of acetaminophen-induced liver injury in mouse

Project description:Acute liver failure (ALF) is a rapidly progressing, life-threatening condition most commonly caused by an overdose of acetaminophen (paracetamol). The antidote, N-acetylcysteine (NAC), has limited efficacy when liver injury is established. If acute liver damage is severe, liver failure can rapidly develop with associated high mortality rates. We have previously demonstrated that alternatively activated macrophages are a potential therapeutic option to reverse acute liver injury in pre-clinical models. In this paper we present data using cryopreserved human alternatively activated macrophages (hAAMs) - which represent a potential, rapidly available, treatment suitable for use in the acute setting. In a mouse model of APAP-induced injury, peripherally injected cryopreserved hAAMs reduced liver necrosis, modulated inflammatory responses, and enhanced liver regeneration. hAAMs were effective even when administered after the therapeutic window for N-acetylcysteine. This cell therapy approach represents a potential treatment for APAP overdose when NAC is ineffective because liver injury is established.

2025-01-29 | GSE280475 | GEO

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