Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Binaprofen induced zebrafish liver injury by mitochondria pathway

ABSTRACT: Binaprofen induced zebrafish liver injury by mitochondria pathway

PROVIDER: PRJNA821454 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18534000.fastq.gz	Fastqsanger.gz
	SRR18534001.fastq.gz	Fastqsanger.gz
	SRR18534002.fastq.gz	Fastqsanger.gz
	SRR18533999.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Binaprofen induced zebrafish liver injury by mitochondria pathway

Project description:Binaprofen induced zebrafish liver injury by mitochondria pathway

| PRJNA821454 | ENA

Binaprofen induced zebrafish liver injury by mitochondria pathway

Project description:The aim was to study the mechanism of liver injury of Binaprofen at genetic level

2022-04-02 | GSE199758 | GEO

Activation of Nrf2/HO-1 signaling pathway exacerbates cholestatic liver injury

Project description:Nrf2 antioxidant signaling is involved in liver protection, but this generalization overlooks conflicting studies indicating that Nrf2 effects are not necessarily hepatoprotective. The role of Nrf2/HO-1 in cholestatic liver injury (CLI) remains poorly defined. Here, we report that Nrf2/HO-1 activation exacerbates liver injury rather than exerts a protective effect in CLI. Inhibiting HO-1 or ameliorating bilirubin transport alleviates liver injury in CLI models. Nrf2 knockout confers hepatoprotection in CLI mice, whereas in non-CLI mice, Nrf2 knockout aggravates liver damage. In the CLI setting, oxidative stress activates Nrf2/HO-1, leads to bilirubin accumulation, and impairs mitochondrial function. High levels of bilirubin reciprocally upregulate the activation of Nrf2 and HO-1, while antioxidant and mitochondria-targeted SOD2 overexpression attenuate the toxicity of bilirubin. Additionally, the expression of Nrf2 and HO-1 is significantly elevated in serum of patients with CLI. These results reveal an unrecognized function of Nrf2 signaling in exacerbating liver injury in cholestatic disease.

2024-04-08 | GSE263093 | GEO

Tissue-resident trained immunity in hepatocytes protects septic-liver injury in zebrafish

Project description:Trained immunity is classically characterized by long-term epigenetic reprogramming of innate immune cells to combat infectious diseases. Infection-induced organ injury is a common clinical severity phenotype of sepsis. However, whether the induction of trained immunity plays a role in protecting septic-organ injury remains largely unknown. Here, through establishing an in vivo β-glucan training and secondary LPS challenge-induced organ injury model in zebrafish larvae, we observe that induction of trained immunity could inhibit the pyroptosis of hepatocytes to alleviate septic-liver injury, with an elevated epigenetic modification of trimethylation at histone 3 lysine 4 (H3K4me3) that targets mitophagy activation. Moreover, we identify a novel C-type lectin domain receptor in zebrafish, named DrDectin-1, which is revealed as the orchestrator in gating H3K4me3 rewiring-mediated mitophagy activation and alleviating the pyroptosis-engaged septic-liver injury in vivo. Taken together, our results uncover a tissue-resident trained immunity in maintaining tissue homeostasis at a whole animal level, and offer a facile in vivo model to efficiently integrate trained immunity for immunotherapies.

2024-04-25 | GSE245156 | GEO

Effect of APAP-induced acute liver injury on WT and Nrf2KO zebrafish liver gene expression following 12 and 24 hours [RNA-Seq]

Project description:To investigate the transcriptional changes following acute liver injury, we exposed WT and Nrf2KO zebrafish larvae to APAP for 12 and 24 hours. We then dissected out zebrafish larval livers and pooled 20 livers per sample for RNA-seq.

2024-01-13 | GSE230829 | GEO

Adipose-derived mesenchymal stem cells inhibit JNK-mediated mitochondrial retrograde pathway to alleviate acetaminophen-induced acute liver injury

Project description:Acetaminophen (APAP) is the major cause of drug-induced liver injury, with limited treatment options. APAP overdose invokes excessive oxidative stress that triggers mitochondria-to-nucleus retrograde pathways, contributing to APAP-induced liver injury (AILI). Mesenchymal stem cell therapy is a promising tool for acute liver failure. Therefore, the purpose of this study is to investigate the beneficial effects of adipose-derived mesenchymal stem cell (AMSC) therapy on AILI and reveal the potential therapeutic mechanisms. C57BL/6 mice are used as the animal model and AML12 normal murine hepatocytes as the cellular model of APAP overdose. Immunohistochemical staining, western blotting, immunofluorescence staining, and RNA sequencing assay are used for assessing the efficacy and validating mechanisms of AMSC therapy. We found AMSC therapy effectively ameliorated AILI, while delayed AMSC injection lost its efficacy related to the c-Jun N-terminal kinase (JNK)-mediated mitochondrial retrograde pathways. We further found that AMSC therapy inhibited JNK activation and mitochondrial translocation, reducing APAP-induced mitochondrial damage. The down-regulation of activated Ataxia telangiectasia mutated (ATM) and DNA damage response proteins in AMSC treated mice liver indicated AMSC blocked the JNK-ATM pathway. Overall, AMSC may be an effective treatment for AILI by inhibiting JNK-ATM mitochondrial retrograde pathway, which improves APAP-induced mitochondrial dysfunction and liver injury.

2022-12-17 | GSE218879 | GEO

Fibroblast growth factor 21 ameliorates cholestatic liver injury via a hepatic FGFR4-JNK pathway

Project description:Cholestasis is characterized by hepatic accumulation of cytotoxic bile acids (BAs), which often subsequentlyleads to liver injury, inflammation, fibrosis, and ultimately liver cirrhosis. Fibroblast growth factor 21 (FGF21) is a liver secreted hormone with pleiotropic effects on the homeostasis of glucose, lipid, and energy metabolism. However, whether hepatic FGF21 plays a role in cholestatic liver injury remains elusive. We found that serum and hepatic FGF21 levels were significantly increased in response to cholestatic liver injury. Hepatocyte-specific deletion of Fgf21 exacerbated hepatic accumulation of BAs, further accentuating liver injury. Consistently, administration of rFGF21 ameliorated cholestatic liver injury in α-naphthylisothiocyanate (ANIT)-treated and Mdr2 deficiency mice. Mechanically, FGF21 activated a hepatic FGFR4-JNK signaling pathway to decrease Cyp7a1 expression, thereby reducing hepatic BAs pool. Our study demonstrates that hepatic FGF21 functions as an adaptive stress-responsive signal to downregulate BA biosynthesis, thereby ameliorating cholestatic liver injury, and FGF21 analogs may represent a candidate therapy for cholestatic liver diseases.

2023-08-19 | GSE240733 | GEO

Lipidomics of zebrafish liver tissues

Project description:Application of an untargeted liquid chromatography- high resolution mass spectrometry platform for lipidomics profiling of zebrafish liver tissues

2022-02-18 | MSV000088860 | MassIVE

Activation of Nrf2/HO-1 signaling pathway exacerbates cholestatic liver injury

Project description:Activation of Nrf2/HO-1 signaling pathway exacerbates cholestatic liver injury

| PRJNA1095826 | ENA

Small RNAs in anti-tuberculosis drug-induced liver injury

Project description:The antimicrobials isoniazid and pyrazinamide, used for the treatment of tuberculosis are known to cause drug-induced liver injury in humans. This limits the effectiveness of tuberculosis treatment, resulting in incomplete cure, relapse and the development of antimicrobial resistance. MicroRNAs are known to be good biomarkers of disease, with the microRNA miR-122 being diagnostic for liver injury. In this study zebrafish larvae were exposed to the anti-tuberculosis drugs isoniazid and pyrazinamide at concentrations which demonstrated liver injury by microscopy and histology. The aim of this study is to understand small RNA changes occurring in anti-tuberculosis drug-induced liver injury and to attempt to identify novel microRNA biomarkers of liver injury.

2023-12-25 | GSE146260 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data