Transcriptome analysis for differentiated gene expression analysis of TU2218, Vactosertib, and Ramucirumab on VEGF-induced endothelial cell anergy condition
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1000926 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description: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.
2023-12-27 | GSE239760 | GEO
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.
2015-11-01 | GSE72731 | GEO
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
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
Project description:The goal of the project is to identify novel therapeutic targets for retinal vascular hyperpermeability. Three condition (Control, VEGF, and Anti-VEGF) sample of mouse retinal tissues were extensively characterized by global proteome profiling.
2016-03-22 | PXD003656 | Pride
Project description:T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.
2013-04-21 | GSE46242 | GEO
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
Project description:T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system. T cell-specific Egr2 deletion was mediated by use of a Cre-expressing adenovirus and a CAR Tg x Egr2flox/flox mouse in which CAR is expressed exclusively in the T cell compartment from a Lck promoter/CD2 enhancer cassette. OVA-specific Th1 cell clones were generated from CAR Tg x Egr2flox/flox mice. CAR Tg x Egr2flox/flox Th1 T cells were infected with an empty (EV) or a Cre-expressing adenovirus. Upon confirmation of Egr2 deletion by immunoblot, the T cells were left untreated (Control) or anergized (Anergic) by immobilized anti-CD3 for 16 hours, and microarray was conducted after 1 day of rest in culture medium. The microarray analysis was performed three times using three sets of independently manipulated samples
2013-04-21 | E-GEOD-46242 | biostudies-arrayexpress
Project description:Transcriptomic analysis of differentiated myoblasts
| PRJNA701390 | ENA
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