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An integrative genome-wide approach supports a direct and collaborative role of ETS and AP-1 transcription factors in maintaining endothelial cell-specific and anti-inflammatory gene expression programs.

Activation of Wnt/β-catenin signaling in endothelial progenitors derived from human pluripotent stem cells partially induces the specialized blood–brain barrier phenotype while the same treatment in matured endothelial cells is less efficacious.

The nuclear membrane protein SUN1 stabilizes endothelial cell-cell junctions far from the nucleus via regulation of microtubule dynamics and Rho GEF-H1 signaling, revealing long-range cellular communication important for vascular development and function.

Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.

Primary endothelial cell cultures contain markedly heterogeneous cell subtypes that exhibit distinct molecular responses to disease-relevant exposures.

Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Single-cell RNA analysis of brain endothelium identifies the angiogenic venous capillary subset and respective resident endothelial progenitors at the origin of CCM lesions, while arterial endothelial cells are unaffected.

Mitochondrial RNAs attach to chromatin and regulate nuclear transcription in endothelial stress response.

EphrinB2/EphB4-mediated regulation of cytoskeletal contractility is a key homeostatic mechanism of lymphatic endothelial cell-cell junction maintenance, and provides a potential target for therapeutic modulation of lymphatic vessel permeability and function.

The proteins Heart of Glass (HEG1) and Rasip1 are both essential for cardiovascular development; and directly bind to each other to guide Rasip1 to endothelial cell junctions to support vascular integrity.