The transcription factor ERG regulates super-enhancers in endothelial cells [ERG siRNA]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA514102 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8428510.fastq.gz | Fastqsanger.gz | |||
| SRR8428511.fastq.gz | Fastqsanger.gz | |||
| SRR8428512.fastq.gz | Fastqsanger.gz | |||
| SRR8428508.fastq.gz | Fastqsanger.gz | |||
| SRR8428509.fastq.gz | Fastqsanger.gz |
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Project description:The transcription factor ERG regulates super-enhancers in endothelial cells [ERG ChIP-seq]
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Project description:The transcription factor ERG regulates super-enhancers in endothelial cells
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Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. Gene expression analysis of human endothelial cells in resting state, treatment with TNFalpha or TNFalpha with the BET bromodomain inhibitor JQ1
2014-09-29 | E-GEOD-53999 | biostudies-arrayexpress
Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. ChIP-Seq for various transcription factors, RNA Polymerase II, and histone modifications in human endothelial cells
2014-09-29 | E-GEOD-53998 | biostudies-arrayexpress
Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. Chem-Seq for the biotinylated small molecule JQ1 in untreated or TNFalpha treated human endothelial cells
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Project description:Super-enhancers are large clusters of transcriptional enhancers that drive expression of genes that control and define cell identity. Improved understanding of the roles super-enhancers play in biology would be afforded by knowing the constellation of factors that constitute these domains and by identifying super-enhancers across the spectrum of human cell types. We describe here the population of transcription factors, cofactors, chromatin regulators and core transcription apparatus that occupy super-enhancers in embryonic stem cells (ESCs) and evidence that super-enhancers are highly transcribed. We then use epigenomic data to produce a catalogue of super-enhancers in a broad range of human cell types. These super-enhancer domains are associated with genes encoding master transcription factors and other components that play important roles in the biology of these cells. Interestingly, sequence variation associated with a broad spectrum of diseases is especially enriched in the super-enhancers of disease-relevant cell types. Furthermore, we find that cancer cells generate super-enhancers at oncogenes and other genes that play important roles in tumor pathogenesis. We discuss these insights and their implications for future study of human health and disease. ChIP-Seq for transcription factors in mouse embryonic stem cells and H3K27ac in Jurkat T-ALL cell line RNA-Seq for mouse embryonic stem cells
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Project description:The ETS transcription factor ERG is a critical transcription factor that establishes and maintains an EC identity program. ERG is downregulated in several chronic vascular diseases, including atherosclerosis, and has been implicated in suppressing endothelial-to-mesenchymal transition (EndMT). However, the dynamic phenotypic and transcriptional consequences of ERG loss in the endothelium is poorly understood. We knocked down ERG using siRNA and compared this transient ERG loss over time to chronic deletion of ERG in a CRISPR/Cas9 deletion line in aortic ECs. RNA-sequencing and ATAC-sequencing revealed profound and dynamic rewiring of endothelial and mesenchymal transcriptional programs. While EC identity was rapidly lost (24 hours knock-down) at the transcriptional level, barrier dysfunction required longer-term knock- down (72 hours). A mesenchymal gene network and enhanced cell migration also required 72 hours to manifest. Loss of ERG was accompanied by a rapid loss of occupancy of ETS motifs and a gain in open chromatin containing AP1 motifs. Inhibition of AP1, washout of ERG siRNA or expression of ERG protein in ERG knock-out cells, demonstrated that EndMT was reversible. Finally, ERG-regulated genes and regulatory elements were associated with human disease, demonstrating that this transcription factor may be a valuable target of future therapies for vascular diseases.
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Project description:The ETS transcription factor ERG is a critical transcription factor that establishes and maintains an EC identity program. ERG is downregulated in several chronic vascular diseases, including atherosclerosis, and has been implicated in suppressing endothelial-to-mesenchymal transition (EndMT). However, the dynamic phenotypic and transcriptional consequences of ERG loss in the endothelium is poorly understood. We knocked down ERG using siRNA and compared this transient ERG loss over time to chronic deletion of ERG in a CRISPR/Cas9 deletion line in aortic ECs. RNA-sequencing and ATAC-sequencing revealed profound and dynamic rewiring of endothelial and mesenchymal transcriptional programs. While EC identity was rapidly lost (24 hours knock-down) at the transcriptional level, barrier dysfunction required longer-term knock- down (72 hours). A mesenchymal gene network and enhanced cell migration also required 72 hours to manifest. Loss of ERG was accompanied by a rapid loss of occupancy of ETS motifs and a gain in open chromatin containing AP1 motifs. Inhibition of AP1, washout of ERG siRNA or expression of ERG protein in ERG knock-out cells, demonstrated that EndMT was reversible. Finally, ERG-regulated genes and regulatory elements were associated with human disease, demonstrating that this transcription factor may be a valuable target of future therapies for vascular diseases.
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