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Acetaminophen overdose reveals protease activated receptor 4 as a low expressing but potent receptor on the hepatic endothelium in mice

ABSTRACT: Acetaminophen overdose reveals protease activated receptor 4 as a low expressing but potent receptor on the hepatic endothelium in mice

PROVIDER: PRJNA1106897 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28867900_1.fastq.gz	Fastqsanger.gz
	SRR28867900_2.fastq.gz	Fastqsanger.gz
	SRR28867901_1.fastq.gz	Fastqsanger.gz
	SRR28867901_2.fastq.gz	Fastqsanger.gz
	SRR28867902_1.fastq.gz	Fastqsanger.gz

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Acetaminophen overdose reveals protease activated receptor 4 as a low expressing but potent receptor on the hepatic endothelium in mice

Project description:There is a paucity of data on how protease-activated receptors (PARs) regulate transcriptional reprogramming. We sought to determine how the expression of two members of the PAR family (PAR1 and PAR4) on hepatic endothelial cells (ECs) influence transcription in the liver after acetaminophen (APAP) overdose. We combined EC-specific translating ribosome affinity purification with next-generation sequencing (EC-TRAPseq) in endothelial-specific Par1 and Par4 knockout mice. This allowed us to gain an in vivo snapshot of how EC gene expression profiles change with APAP overdose and how the loss of endothelial PARs impacts transcriptional reprogramming in hepatic ECs. This approach also provided a high degree of sensitivity for detecting low-expressing transcripts. We found distinct transcriptional changes in APAP-overdosed ECs between endothelial Par1 and Par4 knockout mice.

2024-06-10 | GSE266395 | 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.

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Role of YAP in Liver Regeneration After Acetaminophen Overdose

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

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Affect of liver transcriptome by acute acetaminophen exposure [mRNA]

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

2013-05-03 | GSE42178 | GEO

Affect of liver transcriptome by acute acetaminophen exposure [miRNA]

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

2013-05-03 | GSE42181 | GEO

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]

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Protein S-nitrosylation Restricts Xenobiotic Receptor PXR Hyperactivity and Ameliorates Acetaminophen-induced Liver Injury in Mice

Project description:Drug-induced liver injury (DILI), especially acetaminophen overdose, is the leading cause of acute liver failure. Pregnane X receptor (PXR) is a nuclear receptor and the master regulator of drug metabolism. Aberrant activation of PXR plays a pathogenic role in the acetaminophen hepatotoxicity. Here, we aimed to examine the PXR S-nitrosylation (SNO) in response to acetaminophen. We found that PXR was S-nitrosylated in hepatocytes and the mouse livers after exposure to acetaminophen or S-nitrosoglutathione (GSNO). Mass-spectrometry and site-directed mutagenesis identified the cysteine 307 as the primary residue for SNO-modification. In hepatocytes, SNO suppressed both agonist (rifampicin and SR12813)-induced and constitutively active PXR (VP-PXR) activations. Furthermore, in acetaminophen overdosed mouse livers, PXR protein was decreased at the centrilobular regions overlapping with increased SNO. In PXR-deficient (PXR-/-) mice, replenishing the livers with the SNO-deficient PXR significantly aggravated hepatic necrosis and apoptosis, increased HMGB1 release, and exacerbated liver injury and inflammation. Particularly, we demonstrated that S-nitrosoglutathione reductase (GSNOR) inhibitor N6022 promoted hepatoprotection by increasing the levels of PXR S-nitrosylation. In conclusion, PXR is post-translationally modified by S-nitrosylation in hepatocytes in response to acetaminophen. This modification mitigated the acetaminophen-induced PXR hyperactivity. It may serve as a new target for therapeutical intervention.

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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.

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Scavenger receptor A ameliorates acetaminophen induced hepatic inflammation

Project description:Acetaminophen-induced liver injury (AILI) occurs frequently and can be life threatening. Although AILI is mainly caused by the direct drug cytotoxicity, increasing evidence suggests that the interplay between hepatocytes and immune cells can define this pathogenic process. To further understand the immunoregulatory role of SRA in AILI, we performed RNA-sequencing analysis using hepatic nonparenchymal cells (NPCs) derived from acetaminophen treated WT or SRA-/- mice to demonstrate hepatocyte-extrinsic mechanisms governed by the immune receptor SRA that maintains liver homeostasis upon drug insult.

2023-12-23 | GSE221747 | GEO

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