Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Time series RNA profiling of endotheilal cells in response to atheroprone and atheroprotective flows

PROVIDER: PRJNA357824 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5116960_1.fastq.gz	Fastqsanger.gz
	SRR5116960_2.fastq.gz	Fastqsanger.gz
	SRR5116970_1.fastq.gz	Fastqsanger.gz
	SRR5116970_2.fastq.gz	Fastqsanger.gz
	SRR5116980.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

Time series RNA profiling of endotheilal cells in response to atheroprone and atheroprotective flows

Project description:To profile shear stress-regulated endothelial transcriptomes, we performed RNA-seq with HUVECs subjected to different shear flow conditions, including atheroprotective pulsatile shear (PS, 12±4 dyn/cm2) and atheroprone oscillatory shear (OS, 0.5±4 dyn/cm2), or kept as static control (ST) for four time periods (1, 4, 12 and 24 hours)

2017-05-22 | GSE92506 | GEO

Atheroprotective flow alters EZH2/H3K27me3 dependent transcriptional profile in human endothelial cells

Project description:Atherosclerosis is a focal disease that preferentially develop in the regions of atheroprone disturbed flow, but less in regions of atheroprotective laminar flow. The mechanisms by which atheroprotective laminar flow prevents atherosclerosis at the epigenetic level remain largely unknown. In this study, we observed that laminar flow decreased histone methyltransferase EZH2, which imposes a repressive epigenetic mark of histone 3 lysine 27 trimethylation (H3K27me3) onto target gene promoters, leading to transcriptional silencing. To evaluate the effect of atheroprotective flow on EZH2 and H3K27me3 dependent genome-wide transcriptional profile, we performed RNA-sequencing study on laminar flow and EZH2 siRNA treated human endothelial cells. Venn diagram was used to compare the common regulated genes by both laminar flow and EZH2 depletion. We found atheroprotective flow and EZH2 depletion altere endothelial gene landscape, which include upregulating atheroprotective genes while downregulating pro-atherosclerotic genes.

2017-09-30 | GSE87534 | GEO

Longitudinal shear stress response in human aortic endothelial cells to atheroprone and atheroprotective conditions

Project description:Longitudinal shear stress response in human aortic endothelial cells to atheroprone and atheroprotective conditions

| PRJNA673729 | ENA

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-seq)

Project description:This data set reveals the changes of histone modifications and chromatin accessibility in human umbilical vein endothelial cells (HUVECs) under atheroprotective pulsatile shear (PS), atheroprone oscillatory shear (OS), or with KLF4 overexpression. Using ChIP-Seq, we defined the H3K27ac and H3K4me1 enrichment under PS and OS conditions. Using ATAC-seq, we identified the chromatin accessibility under KLF4 overexpression.

2020-03-11 | GSE128390 | GEO

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ChIP-seq)

2020-03-11 | GSE128389 | GEO

Integrated Proteomics and Metabolomics Analysis Reveals Differential Lipid Metabolism in HUVEC under high and low shear stress

Project description:<div><b>OBJECTIVE:</b> Atherosclerotic plaque development is closely associated with the hemodynamic forces applied to endothelial cells (EC). Among these, shear stress (SS) plays a key role in disease development since changes in flow intensity and direction could stimulate an atheroprone or atheroprotective phenotype. EC under low or oscillatory SS (LSS) shows upregulation of inflammatory, adhesion and cellular permeability molecules. On the contrary, cells under high or laminar SS (HSS) increase their expression of protective and anti-inflammatory factors. The mechanism behind SS regulation of an atheroprotective phenotype is not completely elucidated.</div><div><b>APPROACH and RESULTS:</b> Here we used proteomics and metabolomics to better understand the changes in endothelial cells (HUVECs) under in vitro LSS and HSS that promote an atheroprone or atheroprotective profile and how these modifications can be connected to atherosclerosis development. Our data showed that lipid metabolism, in special cholesterol metabolism, was downregulated in cells under LSS. The LDLR showed significant alterations both at the quantitative expression level, as well as regarding post-translational modifications. Under LSS, LDLR was seen at lower concentrations and with a different glycosylation profile. Finally, modulating LDLR with atorvastatin led to the recapitulation of a HSS metabolic phenotype in EC under LSS.</div><div><b>CONCLUSIONS:</b> Altogether, our data suggest that there is significant modulation of lipid metabolism in endothelial cells under different SS intensities and that this could contribute to the atheroprone phenotype of LSS. Statin treatment was able to partially recover the protective profile of these cells.</div>

2019-07-25 | MTBLS739 | MetaboLights

Influence of endothelial Cx40 under atheroprone and atheroprotective flow

Project description:Influence of endothelial Cx40 under atheroprone and atheroprotective flow

| PRJNA486531 | ENA

Transcriptional adaptations of HUVECs exposed to high and low fluid shear stress

Project description:The goal of this study was to identify gene signatures in HUVECs exposed to atheroprone low laminar shear stress (LSS) or atheroprotective high laminar shear stress (HSS). The obtained data was used to verify that HSS and LSS application induces gene expression patterns similar to more complex pulsatile and oscillatory flow, respectively.

2022-08-19 | GSE211662 | GEO

Longitudinal Transcriptional Response of Endothelial Cells to Shear Stress

Project description:The goal of this study was to find longitudinal transcriptional response of Human Umbilical Vein Endothelial Cells (HUVECs) to pulsatile shear (PS) and oscillatory shear (OS). PS is associated with an atheroprotective endothelial phenotype, while OS is associated with an atheroprone endothelial phenotype. Using RNASeq method (single-ended 50-bp sequencing on Illumina Hi-seq 2000 instrument), we measured the transcriptional response at 10 time-points (1, 2, 3, 4, 6, 9, 12, 16, 20, 24 hr) under PS and OS conditions. Low flow scenario was used as static condition. Two replicates were used for each condition/time-point. Results: Through combining the temporal data on differentially expressed transcription factors and their targets with existing knowledge on relevant functional pathways, we infer the causal relationships between disparate endothelial functions through common transcriptional regulation mechanisms. Our study presents the first comprehensive temporally longitudinal experimental study and mechanistic model of shear stress response. By comparing the relative endothelial expressions of genes between OS and PS, we provide novel insights and an integrated perspective into endothelial cell function in response to differential shear.

2017-10-10 | GSE103672 | GEO

Longitudinal shear stress response in human aortic endothelial cells to atheroprone and atheroprotective conditions

Project description:The goal of this study was to find longitudinal transcriptional response of human aortic endothelial cells (HAECs) to pulsatile shear (PS) and oscillatory shear (OS) and compare them with the responses in human umbilical vein endothelial cells (HUVECs) [GSE103672]. PS is associated with an atheroprotective endothelial phenotype, while OS is associated with an atheroprone endothelial phenotype. Using RNASeq method (single-ended 75-bp sequencing on Illumina Hi-seq 4000 instrument), we measured the transcriptional response at 3 time-points (1, 4, and 24 hrs) under PS and OS conditions. Measurements were also taken under static condition (ST, no flow) at t = 0 hr. Three replicates were used for each condition/time-point. Our results indicate that the responses of HAECs and HUVECs are qualitatively similar for endothelial-function relevant genes and several important pathways with a few exceptions, thus demonstrating that HUVECs can be used as a model to investigate the effects of shear on arterial ECs, with some reservations. Our findings show that HAECs exhibit an earlier response or faster kinetics as compared to HUVECs. The comparative analysis in this study offers new insights into the mechanisms of common and disparate stress responses across these two endothelial cell types.

2021-01-13 | GSE160611 | 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