Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis for differentiated gene expression analysis of TU2218, Vactosertib, and Ramucirumab on VEGF-induced endothelial cell anergy condition

ABSTRACT: Transcriptome analysis of HUVECs treated with TGFβRI or VEGFR2 inhibitors on endothelial cell anergy condition In this study, the dual inhibitory mechanism of TU2218 was identified using an in vitro analysis mimicking the tumor microenvironment and its anti-tumor effects were analyzed using in vivo mouse syngeneic tumor models. TU2218 directly normalized the activity of damaged T lymphocytes and natural killer cells from TGFβ and suppressed the activity and viability of regulatory T cells. The anergy of endothelial cells induced by VEGF stimulation was completely ameliorated by TU2218, an effect not observed with vactosertib, which only inhibits TGFβ signal.

ORGANISM(S): Homo sapiens

PROVIDER: GSE239760 | GEO | 2023/12/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BMP/Taz-Hippo signaling modulates VEGF-mediated angiogenesis

Project description:The BMP/TGFβ-Smad, Notch and VEGF signaling guides formation of endothelial tip and stalk cells. However, the crosstalk of bone morphogenetic proteins (BMPs) and vascular endothelial growth factor receptor 2 (VEGFR2) signaling has remained largely unknown. We demonstrate that BMP family members regulate VEGFR2 and Notch signaling, and act via TAZ-Hippo signaling pathway. BMPs were found to be regulated after VEGF gene transfer in C57/Bl6 mice and in a porcine myocardial ischemia model. BMPs 2/4/6 were identified as endothelium-specific targets of VEGF. BMP2 modulated VEGF-mediated endothelial sprouting via Delta like Canonical Notch Ligand 4 (DLL4). BMP6 modulated VEGF signaling by regulating VEGFR2 expression and acted via Hippo signaling effector TAZ, known to regulate cell survival/proliferation, and to be dysregulated in cancer. In a matrigel plug assay in nude mice BMP6 was further demonstrated to induce angiogenesis. BMP6 is the first member of BMP family found to directly regulate both Hippo signaling and neovessel formation. It may thus serve as a target in pro/anti-angiogenic therapies.

2020-10-07 | GSE82106 | GEO

FGF-dependent regulation of VEGF signaling via transcriptional control of VEGF receptor 2 expression

Project description:Numerous studies have suggested a link between fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) signaling pathways; however the nature of this link has not been established. To evaluate this relationship we investigated VEGF signaling in endothelial cells with disrupted FGF signaling in vitro and in vivo. We find that endothelial cells lacking FGF signaling become unresponsive to VEGF due to down regulation of VEGFR2 expression caused by reduced Vegfr2 enhancer activation, which is in turn caused by reduced activation of Ets family transcription factors. In vivo this manifests in the loss of vascular integrity and morphogenesis. Thus, basal FGF stimulation of the endothelium is required for maintenance of VEGFR2 expression and the ability to respond to VEGF stimulation and accounts for the hierarchic control of vascular formation by FGFs and VEGF. Primary mouse lung endothelial cells were transduced with either Adeno-Null (empty) or Adeno- dominant negative FGF receptor 1 and harvested 24 hours after transduction. Total RNA was extracted and subjected to the analysis using SuperArray GEArray Q Series Mouse Angiogenesis Gene Array. Comparisons were made between treatments.

2011-06-07 | E-GEOD-28483 | biostudies-arrayexpress

FGF-dependent regulation of VEGF signaling via transcriptional control of VEGF receptor 2 expression

2011-06-07 | GSE28483 | GEO

Kinetic analysis of T cell anergy induction

2015-11-01 | GSE72731 | GEO

Anergy Induction

Project description:pooled mRNA (2, 4, 6 hrs) from A.E7 T cells under conditions which promote or inhibit anergy induction Keywords: ordered

2005-02-23 | GSE2323 | GEO

Transcriptome analysis for differentiated gene expression analysis of TU2218, Vactosertib, and Ramucirumab on VEGF-induced endothelial cell anergy condition

Project description:Transcriptome analysis for differentiated gene expression analysis of TU2218, Vactosertib, and Ramucirumab on VEGF-induced endothelial cell anergy condition

| PRJNA1000926 | ENA

βIV-spectrin as a stalk cell-intrinsic regulator of VEGF signaling

Project description:Defective angiogenesis underlies over 50 malignant, ischemic and inflammatory disorders yet long-term therapeutic applications inevitably fail, thus highlighting the need for greater understanding of the vast crosstalk and compensatory mechanisms. Based on proteomic profiling of angiogenic endothelial components, here we report βIV-spectrin, a non-erythrocytic cytoskeletal protein, as a critical regulator of sprouting angiogenesis. Early loss of endothelial specific βIV-spectrin promotes embryonic lethality in mice due to hypervascularization and hemorrhagic defects whereas neonatal depletion yields higher vascular density and tip cell populations in developing retina. During sprouting, βIV-spectrin expresses in stalk cells to inhibit their tip cell potential by enhancing VEGFR2 turnover in a manner independent of most cell-fate determining mechanisms. Rather, βIV-spectrin recruits CaMKII to the plasma membrane to directly phosphorylate VEGFR2 at Ser984, a previously undefined phosphoregulatory site that strongly induces VEGFR2 internalization and degradation. These findings support a distinct spectrin-based mechanism of tip-stalk cell specification during vascular development.

2022-02-04 | PXD026618 | Pride

RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF

Project description:IL-6 family cytokines as OSM and CNTF modify angiogenesis to different degree. This study investigates to which extend treatment of endothelial cells with those cytokines can modify VEGF induced angiogenic reactions. Human umbilical vein endothelial cells (HUVECs) were stimulated for 24h by cytokines followed by RNA harvesting and processed for RNA sequencing.

2022-12-04 | GSE196776 | GEO

Kinetic analysis of T cell anergy induction

Project description:T cell receptor(TCR) engagement in the absence of costimulation leads to a state of T cell tolerance known as anergy. Anergy induction requires new protein synthesis since it is inhibited by cycloheximide. In this experiment, we tried to figure out kinetic properties of the gene expression in anergy induction phase and the subsequent anergy maintenance phase. A.E7 cell, a murine CD4(+) T cell clone, was stimulated with anti-TCR antibody for 0, 2, 4, and 6hrs followed by RNA extraction. For the maintenance phase, A.E7 was stimulated for 16hrs and rested for 5days before RNA extraction.

2015-11-01 | E-GEOD-72731 | biostudies-arrayexpress

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

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