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.
Resting-state capillary blood flow and oxygenation are more homogeneous in the deeper cortical layers, underpinning an important mechanism by which the microvascular network adapts to an increased local oxidative metabolism.
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.
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.
Feedback sensing of the intracellular calcium concentration suffices to reproduce the diversity of ionic conductances underlying normal cardiac electromechanical function in a genetically diverse population of mice.
The earliest steps of tumor initiation in the cerebellum are regulated by critical interactions between pre-tumor cells and stromal cells, which can be manipulated by targeting the Norrin/Frizzled4 signaling axis.
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.
Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.
