Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of human monocytes separated from patients with end-stage renal disease (ESRD) compared to healthy control (HC)

ABSTRACT: End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Despite accumulating evidence that monocytes/macrophages play a pivotal role in the pathogenesis of CVDs in ESRD patients, the current knowledge of transcriptomic signatures of monocytes or macrophages in ESRD patients is very lacking. Therefore, we investigated the transcriptome profiling of monocyte separated from patients with ESRD and HC. To explore the changes of gene expression in ESRD patient-derived monocytes, compared to monocytes from healthy controls, microarray were performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155326 | GEO | 2020/07/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional profiling of human monocytes treated with indoxyl sulfate (IS) or p-cresyl sulfate (PCS)

Project description:End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS), major uremic toxins, are major risk factors involved in the pathology of CVD via adverse effects on endothelial cells and immune cells. Thus, transcriptomic overview of uremic toxin-mediated genes in immune cells of ESRD patients is critical, but not yet fully known. We investigated the alteration of gene expressions and biological pathways mediated by major uremic toxins, in ESRD patients monocytes, via microarray analysis. To explore uremic toxin-related transcriptional profiling in ESRD patient-derived monocytes, purified monocytes from healthy controls were treated with IS or PCS for 24 hr, followed by conducting microarray on these samples.

2020-07-30 | GSE155325 | GEO

Transcriptional profiling of human monocytes separated from patients with end-stage renal disease (ESRD) compared to healthy control (HC)

Project description:Transcriptional profiling of human monocytes separated from patients with end-stage renal disease (ESRD) compared to healthy control (HC)

| PRJNA649415 | ENA

Genomic profiling of 19 renal cell carcinoma samples from patients with end-stage renal disease

Project description:In this study, 19 tumor samples from patients with renal cell carcinoma (RCC)-end-stage renal disease (ESRD) were analyzed by array comparative genomic hybridization (array CGH) using the Agilent Whole Human Genome 4× Array. 19 cystic disease samples from patients with RCC-ESRD

2012-04-01 | E-GEOD-33117 | biostudies-arrayexpress

Gene expressions in human peripheral blood mononuclear cells

Project description:PBMCs were isolated from normal CKD patient, end-stage renal disease patients without HF (ESRD), ESRD patients with HFpEF, and heart failure with reduced ejection fraction (HFrEF). The difference expression genes (DEGs) in PBMCs among different groups were compared using microarray.

2023-12-30 | E-MTAB-13612 | biostudies-arrayexpress

Genomic profiling of renal cell carcinoma in patients with end-stage renal disease

Project description:In this study, eighty tumor samples from 63 patients with renal cell carcinoma (RCC)-end-stage renal disease (ESRD) were analyzed by array comparative genomic hybridization (array CGH) using the Agilent Whole Human Genome 4×44K Oligo Micro Array. 79 tumor samples from 63 patients with RCC-ESRD

2012-03-24 | E-GEOD-28601 | biostudies-arrayexpress

Uremic toxin indoxyl sulfate induces trained immunity via the AhR-dependent arachidonic acid pathway in end-stage renal disease [RNAseq]

Project description:Trained immunity is the long-term functional reprogramming of innate immune cells, which results in altered responses toward a secondary challenge. Despite indoxyl sulfate (IS) being a potent stimulus associated with chronic kidney disease (CKD)-related inflammation, its impact on trained immunity has not been explored. Here, we demonstrate that IS induces trained immunity in monocytes via epigenetic and metabolic reprogramming, resulting in augmented cytokine production. Mechanistically, the aryl hydrocarbon receptor (AhR) contributes to IS-trained immunity by enhancing the expression of arachidonic acid (AA) metabolism-related genes such as Arachidonate 5-Lipoxygenase (ALOX5) and ALOX5 Activating Protein (ALOX5AP). Inhibition of AhR during IS training suppresses the induction of IS-trained immunity. Monocytes from end-stage renal disease (ESRD) patients have increased ALOX5 expression and after 6-day training, they exhibit enhanced TNF-α and IL-6 production to LPS. Furthermore, healthy control-derived monocytes trained with uremic sera from ESRD patients exhibit increased production of TNF-α and IL-6. Consistently, IS-trained mice and their splenic myeloid cells had increased production of TNF-α after in vivo and ex vivo LPS stimulation compared to that of control mice. These results provide insight into the role of IS in the induction of trained immunity, which is critical during inflammatory immune responses in CKD patients.

2024-06-20 | GSE263024 | GEO

Uremic toxin indoxyl sulfate induces trained immunity via the AhR-dependent arachidonic acid pathway in end-stage renal disease [ChIPseq]

2024-06-20 | GSE263019 | GEO

Clonal Haematopoiesis-related Mutant ASXL1 Promotes Atherosclerosis in Mice via Dysregulated Innate Immunity [scRNA-seq]

Project description:Certain somatic mutations confer a fitness advantage in hematopoietic stem cells, resulting in the clonal expansion of mutant blood cells, known as clonal haematopoiesis (CH). Among the top 3 CH mutations, ASXL1 mutations present the highest risk for developing cardiovascular diseases (CVDs). However, how ASXL1 mutations induce CVDs remains totally elusive. Here we show that haematopoietic cells harbouring C-terminally truncated form of ASXL1 mutant (ASXL1-MT) accelerated development of atherosclerosis in Ldlr–/– mice. Transcriptome analyses of plaque-cells showed inflammatory signatures of monocytes and macrophages expressing ASXL1-MT. Mechanistically, wild-type ASXL1 inhibited innate immune signalling through the inhibition of IRAK1-TAK1 interaction in the cytoplasm, indicating an unexpected non-epigenetic role of ASXL1. In contrast, ASXL1-MT lost this regulatory function, leading to NF-κB activation. Intriguingly, IRAK1/4 inhibition decreased inflammatory monocytes and atherosclerosis driven by ASXL1-MT. The present work connects ASXL1 mutations with inflammation and CVDs, giving a clue to prevent CVDs in ASXL1-CH.

2024-10-25 | GSE279601 | GEO

Clonal Haematopoiesis-related Mutant ASXL1 Promotes Atherosclerosis in Mice via Dysregulated Innate Immunity

2024-10-25 | GSE279450 | GEO

Differences in monocyte miRNA profiles between patients with coronary artery disease and healthy controls

Project description:Cardiovascular disease (CVD) is the leading cause of human morbidity and mortality worldwide, underscoring the need to improve diagnostic strategies. Monocytes play a major role in the initiation, propagation, and progression of CVD. MicroRNAs are endogenous small non-coding RNAs that control gene expression and are expressed in a tissue and disease-specific manner. Therefore they have been proposed to be useful biomarkers. The aim of this study was to investigate whether differences in miRNA expression levels in monocytes can be found (i) between patients with premature CVD and healthy controls, (ii) within healthy controls after and before aspirin and statin administration, and (iii) between current, former and non smokers.

2017-10-21 | GSE105449 | 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