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Inflammatory stress-mediated chromatin changes underlie dysfunction in endothelial cells. [ATAC-Seq]

ABSTRACT: Inflammatory stress-mediated chromatin changes underlie dysfunction in endothelial cells. [ATAC-Seq]

PROVIDER: PRJNA1113657 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29089713_1.fastq.gz	Fastqsanger.gz
	SRR29089713_2.fastq.gz	Fastqsanger.gz
	SRR29089714_1.fastq.gz	Fastqsanger.gz
	SRR29089714_2.fastq.gz	Fastqsanger.gz
	SRR29089715_1.fastq.gz	Fastqsanger.gz

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Inflammatory stress-mediated chromatin changes underlie dysfunction in endothelial cells.

Project description:Inflammatory stresses underlie endothelial dysfunction and contribute to the development of chronic cardiovascular disorders such as atherosclerosis and vascular fibrosis. The initial transcriptional response of endothelial cells to pro-inflammatory cytokines such as TNF-alpha is well established. However, very few studies uncover the effects of inflammatory stresses on chromatin architecture. We used integrative analysis of ATAC-seq and RNA-seq data to investigate chromatin alterations in human endothelial cells in response to TNF-alpha and febrile-range heat stress exposure. Multi-omics data analysis suggests a correlation between the transcription of stress-related genes and endothelial dysfunction drivers with chromatin regions exhibiting differential accessibility. Moreover, microscopy identified the dynamics in the nuclear organization, specifically, the changes in a subset of heterochromatic nucleoli-associated chromatin domains, the centromeres. Upon inflammatory stress exposure, the centromeres decreased association with nucleoli in a p38-dependent manner and increased the number of transcripts from pericentromeric regions. Overall, we provide two lines of evidence that suggest chromatin alterations in vascular endothelial cells during inflammatory stresses.

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