Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

ABSTRACT: Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

PROVIDER: PRJNA1188168 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31401861.fastq.gz	Fastqsanger.gz
	SRR31401862.fastq.gz	Fastqsanger.gz
	SRR31401863.fastq.gz	Fastqsanger.gz
	SRR31401864.fastq.gz	Fastqsanger.gz
	SRR31401865.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Flow-cytometric quantification of urine kidney epithelial cells specifically reflects tubular damage in acute kidney diseases

Project description:Despite tubular injury being one of the main mechanisms driving acute kidney injury (AKI), clinicians still have a limited diagnostic repertoire to precisely monitor damage to tubular epithelial cells (TEC). In our previous work we used single cell sequencing to identify TEC subsets as main component of the urine signature in AKI. The aim of this study was to establish TEC as a clinical marker for tubular damage. In total 243 patients were analyzed. For sequencing, we collected eight urine samples of patients with AKI and glomerular disease. By aligning urinary single-cell transcriptomes and TEC-surface proteins using Cellular Indexing of Transcriptome and Epitope Sequencing (CITE-Seq), we developed a protocol for flow cytometric quantification of CD10/CD13+ proximal and CD227/CD326+ distal TEC in urine. The marker combinations were confirmed in kidney biopsies. We validated our approach across four cohorts totaling 235 patients, consisting of patients with AKI (n=63), SARS-CoV-2 infection (n=47), ANCA-associated vasculitis (AAV) with active disease and stable remission (n=110) and healthy controls (n=15). Our findings demonstrate that CD10/CD13 and CD227/CD326 adequately identify proximal and distal urinary TEC, respectively. Distal urinary TEC counts correlate with the severity of AKI based on KDIGO stage and acute eGFR loss in two separate cohorts and can successfully discriminate AKI from healthy controls as well as glomerular disease. We propose urinary CD227/CD326+ TEC counts as a specific, non-invasive marker for tubular injury in AKI. Our protocol provides the basis for a deeper phenotypic analysis of urinary TECs

2025-02-18 | GSE282344 | GEO

Expression data from mice overexpressing Tcfeb specifically in P0 kidney

Project description:In order to identify the effects of Tcfeb overexpression on the kidney transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the double heterozygous KSP_CRE/KSP_Tcfeb mice as compared to control KSP_CRE mice Transcriptome analysis of mice overexpressing Tcfeb specifically in kidney

2016-08-29 | GSE62977 | GEO

Expression data from mice overexpressing Tcfeb specifically in P14 kidney

Project description:In order to identify the effects of Tcfeb overexpression on the kidney transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the double heterozygous KSP_CRE/KSP_Tcfeb 14 days old mice as compared to control KSP_CRE mice Transcriptome analysis of 14 days old mice overexpressing Tcfeb specifically in kidney

2016-08-29 | GSE63376 | GEO

Generation of human kidney organoids from urine cells

Project description:Kidney organoids are ideal models to study the complex process of human kidney development. Here we report the generation of functional kidney organoids by reprogramming human urine epithelial cells (hUCs). RNA-seq and ATAC-seq revealed the three-stage process of the 2D U-iRO induction. Single cell RNA-seq further reveals the cell types in 2D and 3D organoids, 2D U-iRO dominated with mesenchyme and 3D U-iRO with tubule.

2022-10-18 | GSE198844 | GEO

Inflammatory milieu by crosstalk between podocytes and proximal tubular cells in type 2 diabetic kidney disease

Project description:Due to the limited availability of therapeutic agents for type 2 diabetic kidney disease (DKD), there is a need for further knowledge derived from experimental models and innovative techniques. In addressing this issue, single-cell RNA sequencing (scRNA-seq) has been exclusively applied to a genetically modified DKD model, but not an induced model representing type 2 DKD. Herein, we analyzed scRNA-seq and other experiments from an induced type 2 DKD model, and validated the results in human-derived biospecimens. The model was induced by combining a high-fat diet with streptozotocin to simulate induced type 2 DKD. scRNA-seq, histological, and flow cytometric analyses were conducted, and their results were compared with control mice. The findings were then applied to human kidneys exhibiting diabetic glomerulosclerosis associated with type 2 diabetes.

2025-01-01 | GSE261356 | GEO

Generation of human kidney organoids from urine cells (ATAC-seq)

2022-10-18 | GSE198838 | GEO

Generation of human kidney organoids from urine cells (RNA-seq)

2022-10-18 | GSE198839 | GEO

Generation of human kidney organoids from urine cells (scRNA-Seq)

2022-10-18 | GSE198840 | GEO

Analysis of proteome and phosphoproteome of mice kidney with deletion of renal tubular Raptor as compared to control animals

Project description:Raptor expression was specifically deleted in the tubular system of the kidney using an inducible Cre-Lox system under the control of a Pax8 promotor. Please see further details concerning the experimental procedures in the accompanied publication

2016-05-11 | PXD002422 | Pride

Loss of proximal tubular Kruppel-like factor 15 (KLF15) exacerbates kidney injury through loss of fatty acid oxidation

Project description:KLF15 has a critical role in other kidney cell types, but its role in mediating proximal tubular (PT) fatty acid oxidation (FAO) in AKI has not been determined. PT-specific KLF15 knockdown (Klf15PTKO) and control Klf15fl/fl mice were treated with multiple low doses of the PT-specific DNA-damaging agent aristolochic acid I (AAI) and RNA-sequencing of kidney cortex undertaken. Klf15PTKO exhibited worse kidney injury than Klf15fl/fl mice after AAI treatment. Immune system and integrin signaling pathways were significantly upregulated in Klf15PTKO versus Klf15fl/fl mice. Metabolic pathways, specifically FAO, were significantly downregulated in Klf15PTKO versus Klf15fl/fl mice, including PPARalpha signaling.

2023-04-28 | GSE150098 | 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