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.
Improved 3D and 4D imaging of neurovascular processes across scales reveals new insights into eye disease mouse models and shows retinal vessels are significantly distorted using standard flat-mount confocal imaging.
The IL-4/IL-4Rα axis directory promotes pathological angiogenesis through communications with bone marrow cells leading to neovascular age-related macular degeneration.
Cyr61 autoregulating tip cell activity by interlinking integrin and Hippo pathway and targeting Cyr61 provides promising therapeutic approach for the treatment of pathological angiogenesis, including tumour angiogenesis.
Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.
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.
Increasing levels of the growth factor Vegfa disrupt blood vessel branching morphogenesis and drive diameter increase by synchronizing Notch signalling fluctuations between endothelial cells.
Analyses with genetically engineered mouse models in combination with biochemical approaches reveal a crucial role of the receptor tyrosine kinase Tie2 mediated signals in venogenesis via an Akt mediated regulation of COUP-TFII protein stabilization.
Interactions between Neuropilin-1 and VEGFR2, rather than VEGF-Neuropilin-1 binding, underlie Neuropilin-1's critical function in VEGF-mediated vascular development.
