UCL Institute of Cardiovascular Science

VEGF is essential for angiogenesis in development and neoangiogenesis in ischemic pathologies. In adults, it additionally regulates vascular permeability. Our previous research revealed that the differential matrix affinity of VEGF isoforms promotes the formation of chemotactic gradients that guide sprouting vessels to sites of VEGF expression. Current research in the lab seeks to define the signalling pathways that distinguish angiogenic from permeability signalling pathways to open up new avenues for targeted vascular therapies. 

The transmembrane receptor NRP1 binds both class 3 semaphorins and the VEGF164 isoform of VEGF. We previously reported that semaphorin signalling through NRP1 is dispensable for vascular development, but that VEGF164 signalling through NRP1 regulates neuronal migration, survival and commissural axon guidance and cooperates with neural semaphorin signalling to orchestrate the formation of specific neuronal systems. Current research seeks to define the signalling pathways that convey VEGF164/NRP1 signals in neurons and their progenitors. 

We previously showed that VEGF-mediated vessel sprouting synergises with macrophage-promoted sprout fusion to build precisely patterned vessel networks. Current research in the lab seeks to elucidate the molecular mechanisms of macrophage-endothelial cell interactions and the contribution of myeloid cell populations to neoangiogenesis and VEGF-mediated vascular permeability.