Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular pathological mechanism of DIQUAT-induced multi-organ injury

ABSTRACT: Diquat is one of the most commonly used pesticides in recent years, and its improper use can lead to acute poisoning and loss of life. This study employed single-cell and single-cell nucleus transcriptome sequencing on mouse lung, liver, and kidney tissues induced by diquat to unveil the molecular pathophysiology of multi-organ damage caused by diquat exposure. In this research, we emphasize a novel hepatic cell subpopulation associated with detoxification and metabolic dysregulation following diquat exposure in the liver. Furthermore, a robust and intricate immune-inflammatory response is a prominent feature in the lungs, while a time-dependent shift from glomerular infiltration to tubular injury pattern is the main characteristic in the kidneys. This study underscores distinct injury features in multiple organs, significantly enhancing our understanding of diquat-induced multi-organ damage. Relevant molecules and pathways identified may serve as potential novel molecular targets.

ORGANISM(S): Mus musculus

PROVIDER: GSE245687 | GEO | 2024/11/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DCK (diquat)-induced lung injury

Project description:Diquat (DQ) poisoning is a severe medical condition with life-threatening implications and multi-organ dysfunction, yet its underlying mechanism remains incompletely understood. This study unveils a critical process in DQ-induced toxicity. DQ disrupts the mitochondrial genome stability in endothelial cells, leading to the accumulation of Z-form DNA. This triggers an interaction between Z-DNA binding protein 1 (ZBP1) and receptor interacting protein kinase 3 (RIPK3), setting off RIPK3-dependent necroptotic and ferroptotic signaling pathways. Depletion of ZBP1 or RIPK3 in endothelial cells effectively inhibits both necroptosis and ferroptosis, reducing organ damage and mortality. Importantly, we discover that RIPK3 plays a dual role. It phosphorylates MLKL to induce necroptosis and phosphorylates FSP1, inhibiting its enzymatic activity and promoting ferroptosis. The phosphorylation of T163 in FSP1 is crucial for suppressing its activity. Combining the deletion of MLKL with vitamin K treatment proves highly effective in mitigating multi-organ damage and lethality caused by DQ.

2024-03-25 | GSE244858 | GEO

Expression profiling of viologen hebicides in a mouse hepatocyte model

Project description:Paraquat and diquat are viologen herbicides used in commercial agriculture and for residential outdoor weed control. They are related structurally, each containing multiple aromatic rings and two quaternary ammonium cations. Paraquat is one of the most widely used herbicides in the world; however, due to recent toxicity studies and its association with Parkinson’s disease, it is now available only to commercially licensed users in the United States. In contrast, diquat has not been associated with Parkinson’s disease and is available for both commercial and residential applications in the United States. In general, the proposed mechanism by which toxicity occurs following exposure to either herbicide is similar. Both are readily converted to free radicals via the superoxide anion radical and react with molecular oxygen to generate additional redox products that promote oxidative stress and potentially cell death. Diquat is generally considered a safer alternative to paraquat based on its lower incidence of poisoning reports; however, recent work in our lab suggests diquat is significantly more hepatotoxic than paraquat. Studies reporting direct comparisons of paraquat and diquat, especially regarding their potential impact on liver injury, are definitely lacking. The goal of this project is to address this knowledge gap by exposing an in vitro hepatocellular model (TGF-alpha transgenic mouse hepatocytes; TAMH) with each viologen herbicide to further elucidate toxicologic mechanisms and outcomes. The microarray data identified MAPK as an important contributor to diquat-induced toxicity and offers a new generalized approach for broader gene expression-level investigations.

2020-07-08 | GSE153959 | GEO

In vivo transcriptomic responses to thioacetamide exposure in guinea pig liver tissue

Project description:In this study we tested the ability to predict organ injury from transcriptomic data in Hartley guinea pigs at early time points after exposure to thioacetamide (9 and 33 hours). We selected thioacetamide, a compound extensively used in animal studies for its ability to cause liver damage.

2021-03-25 | GSE169545 | GEO

In vivo transcriptomic responses to mercury chloride exposure in rat kidney tissue

Project description:In this study we tested the ability to predict organ injury from transcriptomics data in Sprague-Dawley rats at early time points after exposure to mercury chloride (10 and 34 hours). We selected mercury chloride, a compound extensively used in animal studies for its ability to cause acute kidney and liver damage.

2020-07-07 | GSE147248 | GEO

In vivo transcriptomic responses to thioacetamide exposure in rat liver, kidney, and heart tissue

Project description:In this study we tested the ability to predict organ injury from transcriptomics data in Sprague-Dawley rats at early time points after exposure to thioacetmide (8 and 24 hours). We selected thioacetamide, an organosulfur compound extensively used in animal studies as a hepatotoxin and carcinogen for its ability to cause acute liver damage.

2018-09-20 | GSE120195 | GEO

Project description:diquat induced multiorgan injury

| PRJNA1028283 | ENA

Transcriptional changes in soleus muscle for rats exposed to different activities after contusion injury to the spinal cord and transcriptional changes in soleus muscle with complete spinal cord transection injury

Project description:Spinal cord injury (SCI) is a devastating clinical condition resulting in significant disabilities for affected individuals. Apart from local injury within the spinal cord, SCI patients develop a myriad of complications characterized by multi-organ dysfunction. Disorders, such as lung injury, cardiovascular disease, liver damage, kidney and urinary tract dysfunction, alterations in gut microbiome, neuropathic pain, depression and altered immune responses are common in SCI patients. Such whole body, systemic responses hinder the functional recovery and can be life-threatening in SCI population. Investigations of organ specific gene expression analyses can provide a better understanding of the injury response and identify molecular targets. Consequently, this can be used to develop treatment for SCI, promoting functional recovery and overall quality of life.

2020-04-07 | GSE129694 | GEO

Activity-induced changes in the liver transcriptome after chronic spinal cord injury

2019-04-29 | GSE124819 | GEO

Green tea polyphenols alleviate liver injury induced by di(2-ethylhexyl) phthalate in mice

Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.

2023-10-03 | GSE232128 | GEO

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.

2019-03-20 | GSE111828 | 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