Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA215174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR952346.fastq.gz | Fastqsanger.gz | |||
| SRR952347.fastq.gz | Fastqsanger.gz | |||
| SRR952348.fastq.gz | Fastqsanger.gz | |||
| SRR952349.fastq.gz | Fastqsanger.gz | |||
| SRR952350.fastq.gz | Fastqsanger.gz |
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Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. Examination of NFATc1 and two different histone marks in HUVEC in the presence/absense of VEGF.
2013-09-01 | E-GEOD-49428 | biostudies-arrayexpress
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. To determine NFATc1-regulated genes, a total of 5 samples were derived from human umbilical vein endothelial cells (HUVECs) stimulated with or without 50ng/mL VEGF (VEGF 60min and 0min, respectively), pretreated with cyclosporine A (VEGF 60min plus CsA) and infected with adenovirus expressing the control or constitutively active NFATc1 (Ad-control and Ad-NFATc1).
2013-09-01 | E-GEOD-49426 | biostudies-arrayexpress
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns.
2013-09-01 | GSE49428 | GEO
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns.
2013-09-01 | GSE49426 | GEO
Project description:Global analysis of NFATc1 targets in human vascular endothelial cells
| PRJNA213893 | ENA
Project description:Vascular endothelial growth factor A (VEGF-A) is a master regulator of vascular development and function. Consequently, VEGF-A regulated gene expression programs have been under heavy research. In this study we study the transcriptional regulation of VEGF-A-responsive genes in primary aortic endothelial cells (HAEC) and vein endothelial cells (HUVEC) using genome wide global run-on sequencing (GRO-Seq). We show that half of VEGF-A induced genes display a paused phenotype under basal conditions and are thus poised for rapid gene activation. Promoters of paused genes are distinguished from those of non-paused by higher basal enrichment for active histone marks H3K4me3, H3K9ac and H3K27ac. We also show that nearly 100% of the VEGF-upregulated genes are induced at the level of elongation, whereas 38-53% are also induced at the level of initiation. We also report a comprehensive chromatin interaction map generated in HUVECs using tethered conformation capture (TCC) and characterize chromatin interactions in relation to transcriptional activity. We demonstrate that sites of active transcription are more likely to engage in chromatin looping and identify chromatin compartments enriched for VEGF-regulated genes. Cell-type specific transcriptional activity was also shown to reflect boundaries of chromatin interactions within the HOXA cluster. Collectively, these findings provide new insight into mechanisms behind VEGF-A-regulated transcriptional programs in endothelial cells. ChIP-Seq (H3K4me2), GRO-Seq and HiC profiling was performed in HUVECs and HAECs.
2014-10-27 | E-GEOD-52642 | biostudies-arrayexpress
Project description:The main goal of the project was to identify proteins binding to vascular endothelial growth factor receptor 2 (VEGFR2) phosphorylation site Y1173. Synthetic peptides, phosphorylated or not, covering different tyrosine phosphorylation sites in VEGFR2 were immobilized and incubated with cell lysates from human umbilical vein endothelial cells. Retained proteins were analyzed by mass spectrometry. Proteins specifically binding to pY1173 peptide were categorized with regard to the presence of an Src Homology 2 (SH2) domain and the main hits were validated in intact cells treated or not with VEGF, for their ability to bind to the activated wild type VEGFR2 but not to a mutant Y1173F VEGFR2. The role of the pY1173 binding partners in VEGF-regulated endothelial biology was further examined in vitro and in vivo.
2023-09-19 | PXD041024 | Pride
Project description:Vascular endothelial growth factor A (VEGF-A) is a master regulator of vascular development and function. Consequently, VEGF-A regulated gene expression programs have been under heavy research. In this study we study the transcriptional regulation of VEGF-A-responsive genes in primary aortic endothelial cells (HAEC) and vein endothelial cells (HUVEC) using genome wide global run-on sequencing (GRO-Seq). We show that half of VEGF-A induced genes display a paused phenotype under basal conditions and are thus poised for rapid gene activation. Promoters of paused genes are distinguished from those of non-paused by higher basal enrichment for active histone marks H3K4me3, H3K9ac and H3K27ac. We also show that nearly 100% of the VEGF-upregulated genes are induced at the level of elongation, whereas 38-53% are also induced at the level of initiation. We also report a comprehensive chromatin interaction map generated in HUVECs using tethered conformation capture (TCC) and characterize chromatin interactions in relation to transcriptional activity. We demonstrate that sites of active transcription are more likely to engage in chromatin looping and identify chromatin compartments enriched for VEGF-regulated genes. Cell-type specific transcriptional activity was also shown to reflect boundaries of chromatin interactions within the HOXA cluster. Collectively, these findings provide new insight into mechanisms behind VEGF-A-regulated transcriptional programs in endothelial cells.
2014-10-27 | GSE52642 | GEO
Project description:Endothelial cells (ECs) are phenotypically heterogeneous mainly due to their dynamic epigenetic status. VEGF, the best-known angiogenic factor, activates calcium-NFAT signalling following acute angiogenic gene transcription. Here, we evaluated the global mapping of VEGF-mediated dynamic transcriptional events with a particular focus on major histone-code profiles using ChIP-seq. Remarkably, the regulatory regions of angiogenic transcription factors exclusively acquired embryonic stem-like bivalent histone marks after the VEGF stimulus. Moreover, the newly discovered NFAT-associated epigenome modifier, PTIP in the COMPASS complex, directed gene transcription via MLL3/4-enrichment which overwhelmed the polycomb-brakes. The non-canonical polycomb1 variant, PRC1.3, specifically bound to and allowed the transactivation of PRC2-enriched bivalent angiogenic genes until conventional PRC1 association and gene silencing. Knockdown of these epigenome modifiers abrogated postnatal aberrant neovessel formation via selective inhibition of acute angiogenic bivalent gene transcription. Collectively, the reported dynamic epigenome landscape in ECs may support the development of advanced therapeutic strategies against various vasculopathies.
2021-10-06 | GSE159075 | 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