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

GSE267930 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/05/25 Platform GPL24676
Summary
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.
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Also filed as BioProject PRJNA1113656 and SRA study SRP508793. Searching any of these in the dataset finder brings you back here.

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