Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

VEGF induction of HUVEC and CEP

ABSTRACT: 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 and genes which are differently expressed or VEGF-A induced in HUVEC and CEP, HUVEC and CEP 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22695 | GEO | 2014/12/06

SECONDARY ACCESSION(S): PRJNA128305

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

VEGF induction of HUVEC

2009-09-30 | GSE15464 | GEO

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

Comparison of VEGF versus EGF gene expression in HUVEC

Project description:Angiogenesis is defined as the formation of new capillaries by sprouting from preexisting vessels. It is mainly triggered by vascular endothelial growth factor (VEGF) and occurs in the adult primarily in wound healing processes or in pathologic tumor vessel growth. To identify genes specifically triggered by VEGF and involved in the process of angiogenesis, we utilized Affymetrix microarrays hybridized with cRNA of human umbilical vein endothelial cells (HUVEC) stimulated with either the main trigger of angiogenesis, VEGF or a more general mitogenic growth factor, EGF. This was done under the assumption that, in comparison to EGF, VEGF would induce an additional set of genes not solely required for cell division but necessary for angiogenesis. The obtained data revealed that in HUVEC VEGF induces a large repertoire of genes, the majority of which are not or significantly less induced by EGF. Keywords: time course

2009-06-30 | GSE10778 | GEO

Transcription profiling of HUVEC cells following treatment with angiogenesis trigger, VEGF or a more general mitogenic growth factor, EGF

2009-07-03 | E-GEOD-10778 | biostudies-arrayexpress

Trasncripional regulation by Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

Project description:HUVEC cells were treated with human recombinant VEGF-A165 for either 0h or 18h. A total RNA sample was used for RNA-seq analysis.

2024-03-01 | GSE220505 | GEO

Single-cell trasncripional regulation by Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

Project description:HUVEC cells were treated with human recombinant VEGF-A165 for either 0h or 18h. Whole cells were used for scRNA-seq analysis.

2024-03-01 | GSE235885 | GEO

Slit2 modifies VEGF-induced angiogenic responses in rabbit skeletal muscle by inducing capillary sprouting and decreasing vascular permeability via reduced eNOS activity

Project description:Rationale: Slit2 is a possible modulator of vascular endothelial growth factor (VEGF) - induced angiogenesis, but its effects have not been tested in large animal models. Objective: We studied the effect of Slit2 on therapeutic angiogenesis induced by VEGF receptor 2 (VEGFR2) ligands Vammin and VEGF-DΔNΔC in vivo in rabbit skeletal muscles. The Slit2 target genes were also studied by RNA sequencing (RNA-Seq) in endothelial cells. Methods and Results: Adenoviral intramuscular gene transfers were performed into rabbit hindlimbs. Confocal and multiphoton microscopy were used for blood vessel imaging. Signaling experiments and gene expression analyses were performed to study mechanisms of Slit2 action. Slit2 decreased VEGFR2-mediated vascular permeability. It also reduced VEGFR2-mediated increase in blood perfusion and capillary enlargement, whereas sprouting of the capillaries was increased. Slit2 gene transfer alone did not have any effects on vascular functions or morphology. VEGFR2 activation was not affected by Slit2, but eNOS phosphorylation was diminished. The transcriptome profiling showed Slit2 downregulating angiogenesis-related genes such as nuclear receptor subfamily 4 group A member 1 (NR4A1) and Stanniocalcin-1 (STC-1) as well as genes related to endothelial cell migration and vascular permeability. Conclusions: Combining Slit2 with VEGFs adjusts VEGFR2-mediated angiogenic effects into a more physiological direction. This possibly allows the use of higher VEGF vector doses to achieve a more widespread vector and VEGF distribution in the target tissues leading to a better therapeutic outcome while reducing excess vascular permeability. HUVEC mRNA profiles after adenoviral vector gene transfers in duplicate.

2015-05-26 | E-GEOD-63283 | biostudies-arrayexpress

Homo sapiens

Project description:VEGF induction of HUVEC and CEP

| PRJNA128305 | ENA

Transcriptional profiling to compare genes induced by CYTL1 to genes triggered by VEGF-A under normoxic and hypoxic conditions

Project description:CYTL1 is a bona fide pro-angiogenic factor produced by endothelial colony forming cells (ECFCs), which mediates high angiogenic sprouting of ECFCs and vessel wall endothelial cells by autocrine and paracrine stimulation, respectively. To evaluate whether the signaling response to CYTL1 mimics the response to VEGF-A or induces unique signaling pathways in endothelial cells, we performed transcriptional profiling to compare the gene repertoire induced by CYTL1 to the repertoire triggered by VEGF-A in HUVEC under standard normoxic conditions or angiogensis stimulating hypoxic conditions.

2018-05-01 | GSE71967 | GEO

siRNA-mediated Egr-3 knockdown in VEGF-treated HUVEC

Project description:Analysis of umbilical vein endothelial cells (HUVEC) treated with Egr-3 siRNA under the VEGF treatment for 0,1, and 4 h. Egr-3, a member of early growth response family, is immediately and dramatically induced by VEGF in HUVEC, which regulates expression of many genes related to endothelial activation.

2009-11-30 | GSE18913 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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