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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. We demonstrate that 43% of detected enhancers are EC-specific and contain SNPs associated to cardiovascular disease and hypertension. We provide evidence that AP1, ETS, and GATA transcription factors play key roles in HAEC transcription by co-binding 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 and associate with coordinated binding of CEBPD, IRF1, and NF\u03baB. Collectively, these findings identify cis-regulatory elements and corresponding trans-acting factors that contribute to EC identity and their specific responses to pro-inflammatory stimuli.<\/jats:p>","DOI":"10.7554\/elife.22536","type":"journal-article","created":{"date-parts":[[2017,6,5]],"date-time":"2017-06-05T20:00:11Z","timestamp":1496692811000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.22536","source":"Crossref","is-referenced-by-count":103,"title":["Transcriptional networks specifying homeostatic and inflammatory programs of gene expression in human aortic endothelial cells"],"prefix":"10.7554","volume":"6","author":[{"given":"Nicholas T","family":"Hogan","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B","family":"Whalen","sequence":"additional","affiliation":[{"name":"Department of Cellular 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