Single-cell RNA sequencing reveals extensive endothelial cell (EC) heterogeneity throughout the lung vasculature and identifies two distinct populations, Car4-high ECs and proliferative ECs, that preferentially respond to lung injury.

Endothelial cells in the heart have transcriptional and epigenetic signatures of cardiomyocytes.

In vitro culture of brain endothelial cells leads to a rapid loss of the blood-brain barrier transcriptional and accessible chromatin landscapes that is resistant to the effects of beta-catenin stabilization.

Single-cell transcriptomic analysis reveals novel regenerative endothelial cell populations that mediate remarkably rapid and complete microvascular repair in a novel model of acute lung injury induced by endothelial cell ablation.

A rare population of endothelial cells emerges from a bipotent muscle progenitor population in the paraxial mesoderm and provides niche support to induce hematopoietic stem cells.

Hematopoietic progenitor cells employ CD47 to engage thymic portal endothelial signal regulatory protein alpha for their transendothelial migration and thymic homing.

Genome-wide integration of transcriptome, accessible chromatin, and DNA methylome data from vascular endothelial cells lays the foundation for understanding the gene regulatory circuits that generate organ-specific vascular specialization.

Endothelial dysfunction due to cardiovascular disease risk factors explained by cardiac endothelial cell transcriptome remodelling.

After acute lung injury, the transcription factor Atf3 is essential for regeneration of the capillary endothelium, which is critical for restoring the structure of the lung alveolus.

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.