VE-cadherin is required for trophoblast invasion of the maternal decidua and spiral arteries.

Vascular leakage from pathological vessels in retinopathy aggravates the disease, but endothelial junction stability and barrier integrity can be restored by blocking formation of nitric oxide.

Pathological vessel leakage in mouse retinopathy models depends on VE-cadherin Y685 phosphorylation status, which in turn is regulated by a signaling cascade originating with VEGFR2 Y949 phosphorylation.

The established triple co-culture blood-–brain barrier (BBB) model could be used for predicting drugs’ BBB permeability, and co-culture with neurons and astrocytes enhanced brain endothelial cells’ integrity by secreting GDNF, which upregulated claudin-5 and VE-cadherin expression.

Endothelial YAP/TAZ shape the developing vasculature by orchestrating mechanical inputs with BMP signalling to promote junctional VE-Cadherin turnover and cellular rearrangements.

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

Optogenetic activation of Rho GTPases provides spatiotemporal control over endothelial cell shape and enables control over endothelial barrier function by manipulating the cell-cell overlap with blue light.

Loss of the transcription factor Rreb1 results perturbs epithelial architecture during mouse development resulting in invasive cell behaviors, severe cardiovascular defects, and embryonic lethality.

Analysis of axial polarity distributions shows that Wnt5a regulates collective cell migration in vivo by stabilizing vinculin at adherens junctions and fine-tuning mechanocoupling between neighbouring cells.

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.