Abstract
Endothelial cells 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 in 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 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 NFkB. 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.
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