Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modeling oxidative injury response in human kidney organoids

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE182350 | GEO | 2021/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Modeling oxidative injury response in human kidney organoids

Project description:Modeling oxidative injury response in human kidney organoids

| PRJNA755987 | ENA

Human Pluripotent Stem Cell-Derived Kidney Organoids for Modeling Epithelial Transport and Injury

Project description:Maximizing the potential of human kidney organoids for drug testing, regenerative medicine and to model development and disease requires addressing cell immaturity, the lack of a branching collecting system and the off target cell types. Here we establish methods to independently generate the two kidney progenitor cell populations – metanephric mesenchyme and ureteric bud. Combining these two progenitor cell types results in organoids with an improved branched collecting system. We also identified the hormones aldosterone and arginine vasopressin as critical to promote maturation of collecting duct cell types. The resulting organoids contain the full range of epithelial cells in the nephron, including principal and intercalated cells. By scRNA-seq, we demonstrate superior proximal tubule maturation and reduced off-target cell populations using this protocol.

2020-12-15 | GSE131086 | GEO

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

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

Human Pluripotent Stem Cell-Derived Kidney Organoids for Modeling Epithelial Transport and Injury

Project description:Human Pluripotent Stem Cell-Derived Kidney Organoids for Modeling Epithelial Transport and Injury

| PRJNA542638 | ENA

Evaluation of cisplatin-induced injury in human kidney organoids

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

| PRJNA605973 | ENA

Single cell RNA-seq of iPSC-derived Kidney Organoids treated with TGF-Beta 1 and GSK343 compared with vehicle treated control

Project description:This study used scRNA-seq to characterise the transcriptome in 26 day-old iPSC-derived kidney organoids, treated with TGFB1, the EzH2 inhibitor GSK343, a combination of both or a vehicle control for 48 hours (days 24-26) before harvesting. 2 organoids per condition were pooled and dissociated using a cold-active protease. Nuclei were extracted and profiled using the 10X Genomics Single-cell 3' V3 kits. Libraries were sequenced using paired-end reads on an Illumina NextSeq 500. Initial processing was performed using CellRanger v3.1.0 (10X Genomics).

2023-04-30 | E-MTAB-11138 | biostudies-arrayexpress

Single cell ATAC-seq of iPSC-derived Kidney Organoids treated with TGF-Beta 1 and GSK343 compared with vehicle treated control

Project description:This study used snATAC-seq to profile Chromatin accessibility in 26 day-old iPSC-derived kidney organoids, treated with TGFB1, the EzH2 inhibitor GSK343, a combination of both or a vehicle control for 48 hours (days 24-26) before harvesting. 2 organoids per condition were pooled and dissociated using a cold-active protease. Nuclei were extracted and profiled using the 10X Genomics Single-cell ATAC reagent kit v1.1. Libraries were sequenced using paired-end reads on an Illumina NovaSeq 6000. Initial processing was performed using CellRanger ATAC v1.2.0 (10X Genomics).

2023-04-30 | E-MTAB-11139 | biostudies-arrayexpress

Modeling Genetic Epileptic Encephalopathies using Brain Organoids

Project description:We generated cerebral organoids from genetically engineered human embryonic stem cells (hESCs), modeling the devastating WOREE syndrome (DEE28), as a prototype for genetic epileptic encephalopathies (EEs). Transcriptome analysis of mutated organoids compared to the WT revealed molecular changes related to both early infantile EEs and specifically to WOREE syndrome.

2021-07-01 | GSE156243 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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