ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR539/005/SRR5396645/SRR5396645_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR539/005/SRR5396645/SRR5396645_1.fastq.gzprimaryOK200GenomicsUniversity of Arizonahttps://www.ebi.ac.uk/ena/browser/view/PRJNA381088Endothelial cells (ECs) are critical determinants of vascular homeostasis and inflammation, but transcriptional mechanisms specifying their identities and functional states remain poorly understood. Here, we report a genome-wide assessment of regulatory landscapes of primary human aortic endothelial cells (HAECs) under basal and activated conditions, enabling inference of transcription factor networks that direct homeostatic and pro-inflammatory programs of gene expression. We demonstrate that 43% of detected enhancers are specific to ECs and contain SNPs associated to coronary artery disease (CAD) and hypertension. We provide evidence that AP1, ETS, and GATA transcription factors play key roles in establishing HAEC identity by co-binding at many enhancers associated with EC-specific genes. We further demonstrate that exposure of HAECs to oxidized phospholipids or pro-inflammatory cytokines results in signal-specific alterations in enhancer landscapes that are associated with coordinated binding of CEBPD, IRF1 and NFκB. Collectively, these findings identify cis-regulatory elements and corresponding trans-acting factors that contribute to endothelial cell identity and their specific responses to pro-inflammatory stimuli.xref:EuropePMC:PMC5461113ENAfalseTranscriptional networks specifying homeostatic and pro-inflammatory programs of gene expression in human aortic endothelial cells2023-05-192017-06-17PRJNA381088