Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of endothelial cells derived from Foxo1(+/+) and Foxo1(-/-) ES cells in response to VEGF

ABSTRACT: VEGF induces elongation of endothelial cells (ECs) that are derived from wild-type (Foxo1(+/+)) ES cells. VEGF-induced EC elongation is an important process of angiogenesis. ECs derived from Foxo1(-/-) ES cells fail to elongate in response to VEGF. Gene expression profiling of wild-type and Foxo1(-/-) ECs in the presence or absence of VEGF stimulation identifies responsible genes that regulate EC elongation.

ORGANISM(S): Mus musculus

PROVIDER: GSE76366 | GEO | 2016/02/16

SECONDARY ACCESSION(S): PRJNA307103

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of endothelial cells derived from Foxo1(+/+) and Foxo1(-/-) ES cells in response to VEGF

Project description:VEGF induces elongation of endothelial cells (ECs) that are derived from wild-type (Foxo1(+/+)) ES cells. VEGF-induced EC elongation is an important process of angiogenesis. ECs derived from Foxo1(-/-) ES cells fail to elongate in response to VEGF. Gene expression profiling of wild-type and Foxo1(-/-) ECs in the presence or absence of VEGF stimulation identifies responsible genes that regulate EC elongation. One wild-type (Foxo1(+/+)) ES cell clone and one Foxo1(-/-) ES cell clone were used. ES cells were cultured on OP9 stromal cell layer in the presence or absence of VEGF (10 ng/ml). After 6.5 days, VE-cadherin+ CD31+ ECs were isolated by FACS and used for total RNA extraction. Three independent experiments were performed for each condition.

2016-02-16 | E-GEOD-76366 | biostudies-arrayexpress

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

Trasncripional regulation by FOXO1 in Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

Project description:FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes. Therefore, to identify genes regulated by FOXO1 in long-term VEGF stimulation, we performed RNA-seq analysis of FOXO1-knockdowned human unbilical vein endothelial cells (HUVECs) by siRNA and 18h VEGF treatment.

2024-03-01 | GSE220504 | GEO

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

Genome-wide distribution of histone modification H3K36me3 in ECs during VEGF-signaling

Project description:Vascular endothelial growth factor (VEGF) signaling serves a central role in vascular development as well as maintaining vascular homeostasis. In endothelial cells (ECs), VEGF activates gene expression of angiogenic transcription factors (TFs) followed by downstream induction of angiogenic responsive genes. Recent findings support histone modification dynamics contribute to transcriptional control of genes important for EC functions. Lysine demethylase 2B (KDM2B) demethylates histone H3K4me3 and H3K36me2/3 and also mediates monoubiquitylation of histone H2A119K. KDM2B functions as a transcriptional repressor in somatic cell reprograming and tumor development. However, the role of KDM2B during VEGF-signaling remains to be elucidated. Here, we show in cultured human ECs that knockdown of KDM2B enhances VEGF-induced angiogenesis via increased abilities of migration and proliferation. In contrast, ectopic expression of KDM2B has inhibitory effects on angiogenesis. The function of KDM2B is possibly dependent on its catalytic Jumondi C domain. Genome-wide analysis further reveal that KDM2B selectively controls transcription of VEGF-induced angiogenic TFs where increased H3K4me3/H3K36me3 and decreased of H2A119Kub are associated. These findings suggest an essential role of KDM2B during VEGF-signaling in ECs. Because dysregulation of VEGF signaling in ECs is involved in various diseases including cancer, KDM2B may be a potential therapeutic target in VEGF-mediated vasculopathic diseases.

2022-04-01 | GSE196503 | GEO

RNA-seq analysis to examine the effect of KDM2B knockdown or overexpression on transcriptional responses in ECs during VEGF-signaling

2022-04-01 | GSE196505 | GEO

ChIP-seq analysis for endogenous FOXO1 in human endothelial cells

Project description:FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes. Therefore, to identify genes regulated by FOXO1-binding in long-term VEGF stimulation, we performed ChIP-seq analysis of human unbilical vein endothelial cells (HUVECs) stimulated by VEGF for 18h.

2024-03-01 | GSE220508 | GEO

VEGF promotes RNAPII pausing release through ETS1 to stimulate angiogenesis

Project description:RNA polymerase II (RNAPII) pausing release is a recently recognized checkpoint for transcriptional regulation. The biological roles of RNAPII pausing release and the mechanisms that by which extracellular signals control it are incompletely understood. Here we identify a novel mechanism by which VEGF stimulates RNAPII pausing-release through acetylation of ETS1, a master endothelial cell transcriptional regulator. In endothelial cells (ECs), ETS1 uniquely bound transcribed gene promoters and stimulated their expression by broadly increasing RNA polymerase II (RNAPII) pause release. VEGF enhanced ETS1 chromatin occupancy. Furthermore, VEGF increased ETS1 acetylation, enhancing its binding by BRD4 and thereby stimulating RNAPII pause release. This ETS1-mediated transduction of VEGF signaling to increase RNAPII pausing release was essential for EC angiogenic responses in vitro and in vivo. Together, our results define a new angiogenic pathway in which VEGF enhances ETS1-Brd4 interaction to broadly promote RNAPII pause release and drive angiogenesis.

2016-12-31 | GSE93030 | GEO

Role of microRNAs in Neural Stem Cell-supported Endothelial Morphogenesis

Project description:We checked whether the inhibition of the FGF, VEGF, and TGF signaling pathways would influence the miRNA profile in ECs, co-cultured with NSPCs. EC/NSPC co-cultures were incubated with FGF/VEGF receptor inhibitor PD 173074 (1μM in DMSO), and the TGF-β receptor inhibitor SB431542 (10μM in DMSO, Millipore)

2012-01-01 | E-GEOD-32352 | biostudies-arrayexpress

Transcriptome and epigenetic characterization of ECs during VEGF-signaling

Project description:Transcriptome and epigenetic characterization of ECs during VEGF-signaling

| PRJNA805221 | ENA