Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long RNA in endothelial cells and EVs treated with VEGF or H2O

ABSTRACT: Long RNA in endothelial cells and EVs treated with VEGF or H2O

PROVIDER: PRJNA692230 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13439451.fastq.gz	Fastqsanger.gz
	SRR13439452.fastq.gz	Fastqsanger.gz
	SRR13439453.fastq.gz	Fastqsanger.gz
	SRR13439454.fastq.gz	Fastqsanger.gz
	SRR13439455.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Long RNA in endothelial cells and EVs treated with VEGF or H2O

Project description:RNA was harvested from endothelial cells treated with VEGF or H2O and their associated extracellular vesicles.

2022-03-10 | GSE164868 | GEO

Phosphoproteomic analysis of endothelial cells treated with VEGF and Ang-1

Project description:The phosphoproteomes of bovine aortic endothelial cells (BAECs) treated with VEGF or Angiopoietin-1 for 10min were analyzed using LC-MS/MS.

2016-02-09 | PXD002456 | Pride

Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

Project description:Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

2010-08-17 | E-TABM-765 | biostudies-arrayexpress

Endothelial Rap1B mediates VEGF immunosuppression

Project description:Endothelial Rap1B mediates VEGF immunosuppression

| PRJNA772189 | ENA

MicroRNA expression in HMVECs: control vs. VEGF-treated vs. PEDF/VEGF-treated

Project description:MicroRNA expression profiling of human microvascular endothelial cells (HMVECs) treated with either vascular endothelial growth factor (VEGF) only or in combination with the natural angiogenesis inhibitor pigment epithelial-derived factor (PEDF). Originally we were interested in the microRNA-mediated regulation of angiogenesis by the endogenous anti-angiogenic PEDF. To identify the microRNAs involved in PEDF signaling in activated endothelial cells, we compared the levels of microRNAs in non-treated microvascular endothelial cells, cells treated with VEGF, and cells treated with a combination of VEGF and PEDF. After treatment, total RNA content was isolated and sent for analysis to LC Sciences, LLC. They performed expression profiling and completed statistical analysis, based on which we confirmed the regulation of one of the microRNAs, mir-27b. In the following experiments, we identified the targets of mir-27b relevant for angiogenesis and confirmed our findings in zebrafish and mouse models. The manuscript describes the key role of mir-27b in determination of the endothelial tip cell fate and venous differentiation by regulating Notch ligand Delta-like ligand 4 (Dll4) and Sprouty homologue 2 (Spry2). Three-condition experiment: untreated (control) HMVECs vs. VEGF-treated HMVECs vs. PEDF/VEGF-treated HMVECs.

2011-12-31 | E-GEOD-34735 | biostudies-arrayexpress

Transcription profiling of human umbilical vein endothelial cells (HUVEC) treated with VEGF-A

Project description:Angiogenesis, the formation of new capillaries by sprouting from preexisting vessels, is mainly induced by VEGF-A. To identify genes which are induced by VEGF-A in endothelial cells, HUVEC were starved and induced by VEGF-A165 for 30, 60 and 150min. RNA of induced and uninduced cells was isolated and subjected to microarray analysis using Affymetrix microarray. Experiment Overall Design: Human umbilical vein endothelial cells were grown in complete EGM-2 medium in dense culture for four days without change of medium and before the stimulation in EGM-2 medium without growth factors over night. The cells were stimulated with 100ng/ml VEGF-A165 for 30, 60 and 150 min. RNA was isolated with Trizol according to the manufacturer's instructions.

2009-10-20 | E-GEOD-15464 | biostudies-arrayexpress

Endothelial Rap1B mediates VEGF immunosuppression

Project description:Overcoming vascular immunosuppression: lack of endothelial cell (EC) responsiveness to inflammatory stimuli in the proangiogenic environment of tumors, is essential for successful cancer immunotherapy. The mechanisms through which Vascular Endothelial Growth Factor (VEGF) modulates tumor EC response to exclude T cells are not well understood. The goal was to determine the role of EC Rap1B, a small GTPase that positively regulates VEGF-angiogenesis during development, in tumor growth in vivo. Using mouse models of Rap1B deficiency, Rap1B+/- and endothelial-specific Rap1B KO (Rap1BiΔEC) we demonstrate Rap1B restricts tumor growth and angiogenesis. More importantly, EC-specific Rap1B deletion leads to an altered tumor microenvironment with increased recruitment of leukocytes and increased activity of tumor CD8+ T cells. We find that tumor growth, albeit not angiogenesis, is restored in Rap1BiΔEC mice by depleting CD8+ T cells. Mechanistically, global transcriptome analysis indicated upregulation of the TNF-α signaling and cytokine-induced NFκB transcriptional activity in Rap1B-deficient ECs. In particular, endothelial Rap1B deletion led to upregulation of Cell Adhesion Molecules (CAMs) expression in response to proinflammatory cytokines, and increased interaction with leukocytes in vitro. Importantly, deletion of Rap1 abrogated VEGF-mediated inhibition of CAM expression, demonstrating that Rap1B is essential for mediating VEGF-suppressive signaling. Thus, our studies identify a novel endothelial-endogenous mechanism underlying VEGF-dependent desensitization of EC to pro-inflammatory stimuli. Significantly, they identify EC Rap1 as a potential novel vascular target in cancer immunotherapy.

2022-11-21 | GSE186046 | GEO

MicroRNA expression in HMVECs: control vs. VEGF-treated vs. PEDF/VEGF-treated

2011-12-31 | GSE34735 | GEO

Human dermal lymphatic endothelial cells stimulated with VEGF-A or VEGF-C for 1h, 4h, 8h and 24h

Project description:Lymphatic vessel growth and activation, mediated by vascular endothelial growth factor- (VEGF)-C and/or VEGF-A, play an important role in metastatic cancer spread and in chronic inflammation. We aimed to comprehensively identify downstream molecular targets induced by VEGF-A or VEGF-C in lymphatic endothelium. To this end, we treated human dermal lymphatic endothelial cells (LEC) with VEGF-A or VEGF-C for up to 24 hours, followed by a time-series transcriptional profiling using gene microarray technology. We identified a number of genes - many of them not previously known to be involved in lymphangiogenesis - that clustered either as early response genes, transiently induced genes or progressively induced genes. Endothelial specific molecule-1 (ESM-1) was one of the genes that were most potently induced by both VEGF-A and VEGF-C. Keywords: Time course, growth factor comparison

2008-07-25 | GSE11228 | GEO

Analysis of gene expression changes in endothelial cells upon siRNA of VEGF, Foxo1 or both VEGF+Foxo1

Project description:Analysis of transcriptional changes upon silencing of endothelial VEGF. Because transcription factor Foxo1 levels increase under VEGF silencing, we hypothesized that Foxo1 transcriptional activity would be apparent in a whole-genome microarray. Double-silencing of VEGF+Foxo1 was also performed to determine which transcriptional changes are Foxo1-dependent in a VEGF-deficient background.

2015-12-31 | E-MTAB-2515 | biostudies-arrayexpress

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