Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

ABSTRACT: Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

PROVIDER: PRJNA1087890 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28343902_1.fastq.gz	Fastqsanger.gz
	SRR28343902_2.fastq.gz	Fastqsanger.gz
	SRR28343903_1.fastq.gz	Fastqsanger.gz
	SRR28343903_2.fastq.gz	Fastqsanger.gz
	SRR28343904_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

Project description:COL4A3/A4/A5 mutations have been identified as critical causes of Alport syndrome and other genetic chronic kidney diseases. However, the underlying pathogenesis remains unclear, and specific treatments are lacking. Here, we constructed a transgenic Alport syndrome mouse model by generating a mutation (Col4a3 p.G799R) identified previously from one large Alport syndrome family into mice. We observed that the mutation caused a pathological decrease in intracellular and secreted collagen IV α3α4α5 heterotrimers. The mutant collagen IV α3 chains abnormally accumulated in the endoplasmic reticulum and exhibited defective secretion, leading to persistent endoplasmic reticulum stress in vivo and in vitro. RNA-seq analysis revealed that the MyD88/p38 MAPK pathway plays key roles in mediating subsequent inflammation and apoptosis signaling activation. Treatment with tauroursodeoxycholic acid, a chemical chaperone drug that functions as an endoplasmic reticulum stress inhibitor, effectively suppressed endoplasmic reticulum stress, promoted secretion of the α3 chains, and inhibited the activation of the MyD88/p38 MAPK pathway. Tauroursodeoxycholic acid treatment significantly improved renal function in vivo. These results partly clarified the pathogenesis of renal injuries associated with Alport syndrome, especially in glomeruli, and suggested that tauroursodeoxycholic acid might be useful for the early clinical treatment of Alport syndrome.

2024-08-28 | GSE261588 | GEO

Tauroursodeoxycholic acid-induced neural stem cell proliferation

Project description:Tauroursodeoxycholic acid (TUDCA), an endogenous neuroprotective bile acid and a metabolic regulator, stimulates NSC proliferation and enhances adult NSC pool in vitro and in vivo. In this study, we dissected the mechanism triggered by this proliferation-inducing molecule, namely in mediating metabolic reprogramming. Liquid chromatography coupled with mass spectrometry based detection of differential proteomics revealed that TUDCA reduces the mitochondrial levels of the long-chain acyl-CoA dehydrogenase (LCAD), an enzyme crucial for β-oxidation of long-chain fatty acids (FA).

2021-09-09 | PXD017979 | Pride

Tauroursodeoxycholic acid prevents acute graft-versus-host disease in mice by regulating intestinal apoptosis and inflammation

Project description:The effect of tauroursodeoxycholic acid on the development of acute graft-versus-host disease was tested in a murine allogeneic stem cell transplantation model. TUDCA was shown to reduce acute GVHD by reducing intestinal antigen presentation and following apoptosis and increasing the viability of intestinal epithelial cells.

2021-12-21 | GSE124426 | GEO

Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

Project description:Cells respond to endoplasmic reticulum (ER) stress through activation of signaling pathways such as the Unfolded Protein Response (UPR) which improve the ER folding environment capacity upon changes in misfolded protein burden. Small molecules termed chemical chaperones can attenuate the UPR under stress conditions and improve folding and trafficking of specific mutant proteins. One such compound is the bile acid tauroursodeoxycholic acid (TUDCA). Despite promising results in multiple models of protein folding diseases, TUDCA’s mechanism of action remains unclear. To better define how TUDCA attenuate ER stress, we leveraged the genetically tractable budding yeast, S. cerevisiae. Consistent with properties described for TUDCA, we found it significantly improves growth of yeast subjected to ER stress caused by the N-glycosylation inhibitor tunicamycin (Tm) independently of activity of the UPR. In addition to other data, transcriptomics of strains treated with TUDCA link its ability to resuce Tm-induced stress with cell wall remodeling.

2024-11-13 | GSE186390 | GEO

Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

Project description:Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

| PRJNA773716 | ENA

Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

Project description:Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

| PRJNA986947 | ENA

Blockade of TNFα after ischemia reperfusion injury ameliorates renal prognosis

Project description:Recently, acute kidney injury (AKI) is thought to develop a predisposition toward chronic kidney disease. But the detailed mechanism of the disease progression after AKI is unknown. We made two ischemia-reperfusion injury (IRI) mice models, repaired kidney model and atrophic kidney model, and studied the mechanism that kidney after IRI became atrophy. We found that the atrophy kidney model had two peaks of apoptosis 3 and 14 days after IRI, whereas the repaired kidney model had only one apoptosis peak 3 days after IRI. We showed that the second apoptosis is responsible for the kidney atrophy. Moreover, apoptotic ligands, TNFα and FasL were upregulated at the same time of two apoptosis peaks on the atrophic kidney, and blockade of them before IRI prevented kidney from falling into atrophy. Surprisingly, inhibition of the second apoptosis by anti-TNFα antibody protected from renal atrophy. We propose that apoptosis might play a major role in AKI progression and blockade of TNFα after IRI will be a new therapeutic approach for AKI.

2012-08-10 | GSE39766 | GEO

Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

Project description:Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

| PRJNA934084 | ENA

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

Project description:Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

| PRJNA1108804 | ENA

Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

Project description:The goals of this study is to compare the differently expressed genes in renal tissues of WKY and SHR with or without isoliensinine treatment. The SHRs (n=12) were randomly divided into 2 groups: SHR, and SHR + isoliensinine (5mg/kg/d) groups (n=6 for each group). WKY rats (n=6) were set as control. Rats in WKY and SHR groups were intragastrically with double distilled water (dd H2O); while rats in SHR + isoliensinine (5mg/kg/d) group were intragastrically with 5mg/kg/d of isoliensinine for 10 weeks. Then the renal tissues were used to identify differentially expressed genes among different groups.

2023-09-20 | GSE225146 | 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