Discs large homologue 1 (Dlg1) activates beta-catenin (i.e., canonical Wnt) signaling in CNS endothelial cells to regulate retinal angiogenesis and the development and maintenance of the blood-brain and blood-retina barriers.

Clinical, clinicopathological and image data from Malawian children shows that sequestration in P. falciparum cerebral malaria is visible clinically in the eye as orange retinal vessels and is strongly associated with death.

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.

Experimental analysis of SLC38A5 (solute carrier family 38 member 5) in mouse models and cell culture reveals its novel role as a metabolic regulator of retinal angiogenesis by controlling nutrient uptake and homeostasis in blood vessel endothelium.

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.

Genetic and imaging analysis reveal that microglial precursors use ocular blood vessels as a pathway to enter the optic cup and subsequently infiltrate the retina preferentially through the neurogenic region.

TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.

By using a specialized camera that corrects for eye blur, millions of single-blood-cells are imaged, and their speed measured, as they travel through the largest-to-smallest vessels of the retina.

Targeted manipulations on organotypic cultures show that the retina switches between at least four different metabolic pathways, each with different yields and kinetics, to dynamically adapt to momentaneous energy needs.

Mouse models in which hypoxia can be genetically triggered in retinal pigmented epithelial cells show that hypoxia-induced metabolic stress alone can lead to photoreceptor atrophy/dysfunction.