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Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [circRNA_APAP]

ABSTRACT: Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE241509 | GEO | 2023/09/01

REPOSITORIES: GEO

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Transcriptomic profiling of differentially expressed mRNA in liver tissue of Dgaln/LPS induced liver injury mice [mRNA_Dgaln]

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Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [mRNA_APAP]

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2023-09-01 | GSE241511 | GEO

Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [miRNA_APAP]

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2023-03-11 | PXD036682 | Pride

Transcription profiling of 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. Experiment Overall Design: After a single administration of high dose (300 mg/kg i.p.) APAP, liver and blood samples were extracted from 3 sensitive (C57B6, DBA/2, and SmJ) and 1 resistant (SJL) mice strains at 0, 3 and 6 hour after APAP exposure. Endogenous metabolites from liver samples were analyzed by 1H-13C 2-dimensional-NMR and gene expression changes occurring within these liver samples were simultaneously analyzed using Affymetrix microarrays. The transcriptional and metabolomic data was jointly analyzed, and functional information within the Gene Ontology database was used to identify the subset of genes that could affect susceptibility to APAP-induced liver injury in the early phase response.

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