Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Establishment of epithelial inflammatory injury model using adult kidney organoids [RNA-seq]

ABSTRACT: Establishment of epithelial inflammatory injury model using adult kidney organoids [RNA-seq]

PROVIDER: PRJNA1081385 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28122712_1.fastq.gz	Fastqsanger.gz
	SRR28122712_2.fastq.gz	Fastqsanger.gz
	SRR28122713_1.fastq.gz	Fastqsanger.gz
	SRR28122713_2.fastq.gz	Fastqsanger.gz
	SRR28122714_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Establishment of epithelial inflammatory injury model using adult kidney organoids [scRNA-seq]

Project description:Kidney organoids are emerging as an increasingly applied model system to hold great promise for transplantation to individuals with end-stage renal disease and as a useful tool for kidney research. Multiple iPSC-derived renal organoids have been established to understand kidney development and disease. However, few disease models originated from adult renal tissue with fully mature cell fates have been set up to recapitulate kidney inflammation or fibrosis. Here we created a novel organoid model that faithfully representing the cellular state of inflammatory response during the progression of renal disease upon TNFα exposure. scRNA-seq showed signatured inflammatory chemokines, cytokines and inflammation-associated signaling pathways were activated in TNFα-treatment organoids together with injury-associated markers such as LCN2 and CLU. Donor age is associated with TNFα-induced inflammatory reaction in organoids. Kidney organoids from young donors showed more transcriptional changes by down-regulation of TGFβ and extracellular matrix genes. In summary, we established an in vitro TNFα-treated kidney organoid model that representing the cellular state of the inflammatory response during renal disease progression and provided a novel tool for studying inflammation-related kidney disease and drug discovery.

2024-03-03 | GSE259381 | GEO

Establishment of epithelial inflammatory injury model using adult kidney organoids [RNA-seq]

2024-03-03 | GSE259376 | GEO

Establishment of epithelial inflammatory injury model using adult kidney organoids [scRNA-seq]

Project description:Establishment of epithelial inflammatory injury model using adult kidney organoids [scRNA-seq]

| PRJNA1081386 | ENA

Establishment of epithelial inflammatory injury model using adult kidney organoids.

Project description: Not available

| S-EPMC11749467 | biostudies-literature

Modeling oxidative injury response in human kidney organoids

Project description:Analysis of human kidney organoids treated with hemin for 48 hrs, to induce reactive oxygen injury.

2021-12-31 | GSE182350 | GEO

Modeling oxidative injury response in human kidney organoids

Project description:Modeling oxidative injury response in human kidney organoids

| PRJNA755987 | ENA

Hypoxic injury triggers maladaptive repair in human kidney organoids [scRNA-seq]

Project description:Reduction in blood supply to the kidneys occurs to certain extent during acute kidney injury (AKI). Individuals who suffered AKI are at risk of developing chronic kidney disease (CKD) through a maladaptive repair process. Currently, the lack of a reliable research model that allows the characterization of the maladaptive regeneration during such transition, impedes the development of effective therapies. Here, we present the first human kidney organoid model that physiologically and morphologically resembles the AKI and the maladaptive regeneration. Kidney organoids were generated from human induced pluripotent stem cells. After 18 days of grow the organoids were under hypoxic conditions for 2 days to simulate AKI. Organoids were collected at day 20 to assess hypoxic injury, and after a 5-day recovery in normoxic conditions to assess maladaptive repair. The transcriptome, proteome and metabolome were profiled. Gene expression analysis of day 20 hypoxic organoids identified signatures of injury, cell death (necroptosis and ferroptosis), cell cycle arrest and changes in metabolism. The maladaptive repair phenotype was supported by enrichment of pathways associated with inflammatory signals, oxidative stress, and tissue remodelling. Specific genes associated with kidney injury and disease such as GDF15, MMP7, ICAM1, TGFB1, CCN1, C3 and S100A8/9 were upregulated. Single-cell RNA sequencing localized expression of maladaptive repair genes and activation of TNF and JAK-STAT signalling pathways specific to tubular epithelial cells. Dysregulation in metabolic pathways such as glycolysis and gluconeogenesis, amino acid and lipid metabolisms were conserved in this model. Altogether, these results support the use of kidney organoids as a model of AKI and early CKD that can be used for biomarker validation, elucidation of pathological mechanisms, and drug screening.

2025-08-15 | GSE242425 | GEO

Evaluation of cisplatin-induced injury in human kidney organoids

Project description:Evaluation of cisplatin-induced injury in human kidney organoids

| PRJNA605973 | ENA

Hypoxic injury triggers maladaptive repair in human kidney organoids

Project description:Hypoxic injury triggers maladaptive repair in human kidney organoids

| PRJNA1013401 | ENA

Evaluation of cisplatin-induced injury in human kidney organoids

Project description:Acute kidney injury (AKI) remains a major global healthcare problem and there is a need to develop human-based models to study AKI in vitro. Towards this goal, we have characterized induced pluripotent stem cell-derived human kidney organoids and their response to cisplatin, a chemotherapeutic drug that induces AKI and preferentially damages the proximal tubule. We found that a single treatment with 50 µM cisplatin induces HAVCR1 and CXCL8 expression, DNA damage (γH2AX) and cell death in the organoids in a dose-dependent manner but greatly impairs organoid viability. DNA damage was not specific to the proximal tubule but also affected the distal tubule and interstitial cell populations. This lack of specificity correlated with low expression of the proximal tubule-specific SLC22A2/OCT2 transporter for cisplatin. To improve viability, we developed a repeated low-dose regimen of 4x 5 µM cisplatin over 7 days and found this causing less toxicity while still inducing a robust AKI response that included secretion of known AKI biomarkers and inflammatory cytokines. This work validates the use of human kidney organoids to model aspects of AKI, with the potential to identify new AKI biomarkers and develop better therapies.

2020-02-29 | GSE145085 | 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