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H3K4me3 HiChIP of immortalized human aortic endothelial cells treated with TNFα against untreated controls

ABSTRACT: H3K4me3 HiChIP of immortalized human aortic endothelial cells treated with TNFα against untreated controls

PROVIDER: PRJEB56342 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10292109_1.fastq.gz	Fastqsanger.gz
	ERR10292109_2.fastq.gz	Fastqsanger.gz
	ERR10292110_1.fastq.gz	Fastqsanger.gz
	ERR10292110_2.fastq.gz	Fastqsanger.gz
	ERR10292111_1.fastq.gz	Fastqsanger.gz

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H3K4me3 HiChIP of immortalized human aortic endothelial cells treated with TNFα against untreated controls

Project description:TNFα is a potent cytokine to mediate inflammatory response by activation of the master transcription factor NF-kB. Endothelial cells are important participants in inflammatory responses in animals. NF-kB is a major mediator to activate endothelial cells by inducing multiple pro-inflammatory genes in response to TNFα. The process of transcriptional activation is dependent on the context of chromatin interactions/loops. However, the chromatin conformation in response to the cytokine challenge TNFα in human aortic endothelial cells has not been described. Our approach characterized chromatin interactions from active enhancers to promoters as well as active promoters to promoters on a genome-wide scale and highlighted important enhancer candidates for target genes.

2023-03-01 | E-MTAB-12213 | biostudies-arrayexpress

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Project description:TNFα is a potent cytokine to mediate inflammatory response by activation of the master transcription factor NF-kB. Endothelial cells are important participants in inflammatory responses in animals. NF-kB is a major mediator to activate endothelial cells by inducing multiple pro-inflammatory genes in response to TNFα. NF-kB mediated gene transcription is known to accompany rapid changes in epigenetic states. However, the epigenetic landscape in response to the cytokine challenge TNFα in mouse endothelial cells has not been described. Our approach characterized the epigenetic profiles on a genome-wide scale and mapped putative active enhancers in primary mouse aortic endothelial cells.

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Project description:To identify conserved TNFα-induced changes in chromatin-accessibility in mammals, we performed ATAC-seq in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. We overlay our data with multi-species NF-κB binding data and identify multiple modes of NF-κB-chromatin interactions that are conserved during mammalian TNFα response. Our cross-species approach identifies conserved changes in chromatin-accessibility at NF-κB binding sites that are disease-relevant and essential during mammalian acute inflammation.

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Project description:TNFα has an evolutionary conserved role in mediating inflammation via activation of the transcription factor NF-κB. The functions of individual NF-κB binding sites are not well understood. To identify conserved and functionally important NF-κB binding sites in mammals, we performed ChIP-seq to map the genome-wide binding of RELA and select histone modifications in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. The conserved RELA binding sites show strong epigenetic changes in response to TNFα and enrich near genes controlling vascular development and pro-inflammatory responses. Our method identifies novel modes of RELA-chromatin interactions that are conserved in mammals and shared between multiple cell-types. Particularly, genomic regions bound by RELA prior to stimulation are important responders during TNFα stimulation. We use CRISPR/Cas9 genome editing to validate the roles of the conserved RELA pre-bound sites near pro-inflammatory genes such as CCL2 and PLK2. Our evolutionary approach describes new aspects of mammalian NF-κB biology including its role within super-enhancers and relevance in inflammatory disorders.

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