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Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC-seq]

GSE298902 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2025/11/06 Platform GPL34295
Summary
Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the epigenetic and transcriptional basis of endothelial inflammatory memory, we employed transcriptomic profiling of primary endothelial cells exposed to inflammatory stimuli in a two-hit model. This study reveals persistent transcriptional reprogramming following IL-6 exposure and identifies a primed endothelial state that amplifies responses to secondary challenges.
Published in
Endothelial cells retain inflammatory memory through chromatin remodeling in a two-hit model of infection-induced inflammation
Gonsales Spindola D, Bahr A, Clark S et al. · American journal of physiology. Cell physiology 2025 · PMID 41217002 · doi:10.1152/ajpcell.00567.2025
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Also filed as BioProject PRJNA1271585 and SRA study SRP589670. Searching any of these in the dataset finder brings you back here.

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