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Transcriptomic Profiling of Myeloid Cells in Acetaminophen-Induced Acute Liver Failure

ABSTRACT: Transcriptomic Profiling of Myeloid Cells in Acetaminophen-Induced Acute Liver Failure

PROVIDER: PRJNA1186238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31357143_1.fastq.gz	Fastqsanger.gz
	SRR31357143_2.fastq.gz	Fastqsanger.gz
	SRR31357144_1.fastq.gz	Fastqsanger.gz
	SRR31357144_2.fastq.gz	Fastqsanger.gz
	SRR31357145_1.fastq.gz	Fastqsanger.gz

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Transcriptomic Profiling of Myeloid Cells in Acetaminophen-Induced Acute Liver Failure

Project description:In the recent study, we found that mesenchymal stem cell (MSC)-derived extracellular vesicles expressing the SIRPα protein (SIRP-EVs) were significantly distributed within myeloid cells (CD11b+ cells) and kupffer cells (CD11b+/F4/80+ cells) in acetaminophen (APAP)-induced mouse acute liver failure (ALF) model. Furthermore, SIRP-EVs enhanced the phagocytic activity of macrophages by blocking CD47 on necroptotic hepatocytes and promoted liver regeneration. Therefore, we investigated the therapeutic effects of SIRP-EVs on CD11b+ cells in APAP-induced ALF conditions. CD11b+ cells in the liver, including resident and recruited CD11b+ cells, were harvested and analyzed through bulk RNA sequencing.

2025-01-13 | GSE281951 | GEO

Gene expression profiling in acute liver failure versus healthy human liver

Project description:To understand key pathways and regulatory genes in acetaminophen induced Acute Liver Failure (ALF) for pathophysiological and therapeutic mechanisms gene expression was analyzed and significantly up and down regulated genes were identified

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

Project description: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.

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

2023-09-01 | GSE241510 | GEO

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

2023-09-01 | GSE241509 | GEO

Proteomics Indicates Lactate Dehydrogenase is Prognostic in Acetaminophen-induced Acute Liver Failure Patients and Reveals a Role for LKB1-AMPK Signaling

Project description:Better biomarkers to predict death early in acute liver failure (ALF) are needed. To that end, we obtained early (study day 1) and later (day 3) serum samples from transplant-free survivors (n=28) and non-survivors (n=30) of acetaminophen (APAP)-induced ALF from the NIH-sponsored Acute Liver Failure Study Group, and from control volunteers (n=10). To identify proteins that increase early in serum during ALF, we selected individuals from this cohort for whom ALT was lower on day 1 than day 3, indicating a time point before the peak of injury (n=10/group). We then performed untargeted proteomics on their day 1 samples. Out of 1,682 quantifiable proteins, 79 were elevated ≥4-fold in ALF patients vs. controls and 23 of those were further elevated ≥4-fold in non-survivors vs. survivors, indicating potential to predict death. Interestingly, the biomarker with best performance was LDH. To confirm the prognostic potential of LDH, we measured activity in all day 1 and 3 samples from all 58 ALF patients. LDH was elevated in the non-survivors vs. survivors on both days. In addition, receiver operating characteristic (ROC) curve analyses revealed that LDH alone performed similarly to the model for end-stage liver disease (MELD), while a combination of MELD and LDH outperformed either alone. Finally, Upstream Analysis of our proteomics data indicated activation of LKB1-AMPK signaling in liver regeneration after APAP overdose and we confirmed that in mice. Overall, we conclude LDH can predict death in APAP-induced ALF and that LKB1-AMPK signaling may be a promising therapeutic target to improve survival.

2022-08-12 | PXD029576 | Pride

Transcriptional analysis of in vivo responses to acetaminophen induced hepatic injury in the murine liver

Project description:Liver injury results in rapid regeneration through hepatocyte proliferation and hypertrophy. However, after acute severe injury, such as acetaminophen poisoning, effective regeneration may fail. We investigated how senescence underlies this regenerative failure. In human acute liver disease, and murine models, p21-dependent hepatocellular senescence was proportionate to disease severity and was associated with impaired regeneration. In an acetaminophen injury model a transcriptional signature associated with the induction of paracrine senescence is observed within twenty four hours, and is followed by one of impaired proliferation. In genetic models of hepatocyte injury and senescence we observed transmission of senescence to local uninjured hepatocytes. Spread of senescence depended upon macrophage derived TGFβ1 ligand. In acetaminophen poisoning inhibition of TGFβ receptor 1 (TGFβR1) improved survival. TGFβR1 inhibition reduced senescence and enhanced liver regeneration even when delivered after the current therapeutic window. This mechanism, in which injury induced senescence impairs regeneration, is an attractive therapeutic target for acute liver failure.

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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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