Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [miRNA-Seq]

ABSTRACT: High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [miRNA-Seq]

PROVIDER: PRJNA704558 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13776323.fastq.gz	Fastqsanger.gz
	SRR13776324.fastq.gz	Fastqsanger.gz
	SRR13776325.fastq.gz	Fastqsanger.gz
	SRR13776326.fastq.gz	Fastqsanger.gz
	SRR13776327.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [miRNA-Seq]

Project description:High-throughput Sequencing has revolutionized system-based analysis of cellular pathways. The goals of this study are to find the effect of quercetin pretreatment on the transcriptome of ox-LDL injured endothelial cells

2024-02-24 | GSE167392 | GEO

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [ncRNA-Seq]

2024-02-24 | GSE167391 | GEO

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage

Project description:High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage

| PRJNA704554 | ENA

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [ncRNA-Seq]

Project description:High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [ncRNA-Seq]

| PRJNA704559 | ENA

Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

Project description:We have employed transcriptome microarray expression profiling as a discovery platform to figure out the pharmacological mechanisms of quercetin against endothelial senescence induced by ox-LDL in vitro. Expression of RCHY1, EIF4E1B, IGFBP3, SERPINE1, BRAF, SLC5A11 from this signature was quantified in the same kind of samples by real-time PCR, confirming the change pattern.

2019-10-29 | GSE139288 | GEO

Expression data from ARPE-19 cells treated with LDL or ox-LDL

Project description:LDL or Ox-LDL 200ug/ml, which showed no loss of viability after a 48 hour exposure, induced a physiological and pathological transcriptional response, respectively. LDL induced a downregulation of genes associated with cholesterol biosynthesis while ox-LDL induced transcriptional alterations in genes related to inflammation, matrix expansion, lipid metabolism and processing, and apoptosis. Pentraxin-3 was secreted into the culture medium after RPE cells were stimulated with ox-LDL, and immunohistochemically evident in Bruchs membrane of human macular samples with age-related macular degeneration. ARPE-19 cells exposed to 200ug/ml ox-LDL had a 38% apoptosis rate compared to less than 1% when exposed to LDL or untreated controls (p<0.0001). While LDL induced a physiologic response by RPE cells, a pathological phenotypic response was seen after treatment with oxidatively modified LDL. The transcriptional, biochemical, and functional data provide initial support of a role for the hypothesis that modified LDLs are one trigger for initiating events that contribute to the development of age-related macular degeneration. Keywords: treatment with non-treatment control Human ARPE-19 cells were exposed to LDL or oxidatively modified LDL (ox-LDL) for 48 hours for RNA extraction and hybridization on Affymetrix microarrays. We sought to determine whether retina, pigment epithelial cells develop a pathologic phenotype after exposure to low density lipoproteins (LDL) that are oxidatively modified.We have made two comparsions: LDL treatment versus non-treatment; ox-LDL treatment versus non-treatment.

2006-09-01 | E-GEOD-5741 | biostudies-arrayexpress

Expression data from ARPE-19 cells treated with LDL or ox-LDL

Project description:LDL or Ox-LDL 200ug/ml, which showed no loss of viability after a 48 hour exposure, induced a physiological and pathological transcriptional response, respectively. LDL induced a downregulation of genes associated with cholesterol biosynthesis while ox-LDL induced transcriptional alterations in genes related to inflammation, matrix expansion, lipid metabolism and processing, and apoptosis. Pentraxin-3 was secreted into the culture medium after RPE cells were stimulated with ox-LDL, and immunohistochemically evident in Bruch’s membrane of human macular samples with age-related macular degeneration. ARPE-19 cells exposed to 200?g/ml ox-LDL had a 38% apoptosis rate compared to less than 1% when exposed to LDL or untreated controls (p<0.0001). While LDL induced a physiologic response by RPE cells, a pathological phenotypic response was seen after treatment with oxidatively modified LDL. The transcriptional, biochemical, and functional data provide initial support of a role for the hypothesis that modified LDLs are one trigger for initiating events that contribute to the development of age-related macular degeneration. Keywords: treatment with non-treatment control

2006-09-01 | GSE5741 | GEO

RNA-Sequencing Analysis of ox-LDL-treated Peritoneal Macrophages Transcriptomes

Project description:Since previous stduies demostrated that oxidized phospholipids function as caspase-11 agonists to induce noncanonical inflammasome activation in immune cells and the levels of oxidized phospholipids derived from ox-LDL are largely elevated in atherosclerotic lesions. Purpose:RNA-Sequencing analysis of ox-LDL-treated peritoneal macrophages transcriptomes.Methods and results:The principal component analysis gene expression profiles of the control and ox-LDL-treated groups were clearly distinct. Among the DEGs that met the cutoff criteria of a -log10(false discovery rate (FDR)) > 2 and |log2(fold change (FC)| > 2. A total of 1,388 downregulated and 855 upregulated genes were identified. GSEA showed that the dominant upregulated pathways in ox-LDL-treated macrophages were associated with the IL-1-mediated signaling pathway, response to cytokine stimulus, and granulocyte migrationwe discovered that caspase-11-mediated inflammation signaling was significantly activated in ox-LDL-treated peritoneal macrophages.Conclusions：we verified caspase11associated inflammatory signaling was significantly activated in ox-LDL-treated macrophages.

2021-05-19 | GSE171413 | GEO

Expression data of human vascular smooth muscle cells (hVSMC) in response to n-LDL and ox-LDL.

Project description:Early transcriptomic response to n-LDL and ox-LDL in human vascular smooth muscle cells (hVSMC). We used microarrays with the aim of assessing early molecular changes that induce a response in the VSMC using native and oxidized low-density lipoprotein (n-LDL and ox-LDL).

2016-02-09 | GSE68021 | GEO

Expression data from bladder cancer cells T24 treated with ox-LDL or vehicle

Project description:Target genes regulated by ox-LDL treatment in bladder cancer cells T24 were identified by microarrays. In this dataset, we include the expression data obtained from bladder cancer cells T24 starved with serum-free medium and then treated with 20 μg/mL ox-LDL or vehicle for 24 h. These data are used to obtain genes that are differentially expressed in response to ox-LDL treatment.

2022-02-18 | GSE134530 | 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