Shortage of blood-borne apolipoprotein-M–bound sphingosine-1-phosphate, which accompanies various brain disorders, causes paracellular leak and increase in transcytosis at the blood–brain barrier, which can be reversed, thus is of clinical relevance.

Neuronal activity modulates blood–brain barrier permeability, influencing synaptic plasticity and local network reorganization in the healthy brain.

Matrix metalloprotease (MMP)-14 cleaves Tie2 at three distinct sites within the fibronectin type-III (FN3) domain and its pharmacological blockade inhibits Tie2 pathological shedding to exert barrier protective effects.

Occluding-junctions form a permeability barrier around the hematopoietic niche in Drosophila that controls the production of immune cells in response to infection by shaping the signalling micro-environment produced by the niche.

Elevating beta-catenin signaling converts endothelial cells in typically fenestrated central nervous system vasculature to a blood-brain barrier (BBB) phenotype and promotes a BBB gene expression program and chromatin landscape.

A human stem cell-derived in vitro model provided novel insights into the mechanisms of retinoid accumulation in, and permeation across, the blood–brain barrier.

Endothelial tightening by augmenting low level Wnt/β-catenin activity in vessels of the mouse subfornical organ, influences neuronal activation in water-deprived mice, linking endothelial barrier properties to neuro-vascular coupling.

The invasion of Toxoplasma to the CNS across cortical capillaries is restricted by the integrity of the blood-brain barrier (BBB) and exacerbated by the inflammatory response.

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.

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.