How does NRP2 keep blood vessels sealed and calm under stress? (ROBINSON_Q27DTP)

Blood vessels are lined by endothelial cells, which form a living barrier between blood and tissues. These cells must stay tightly connected, sense blood flow, respond to nutrients and communicate with immune cells, while avoiding unnecessary inflammation. How endothelial cells maintain this stable “barrier identity” during stress is still not fully understood.

This PhD project will investigate neuropilin-2, or NRP2, a cell-surface receptor best known for roles in blood vessel development. Our new data suggest that NRP2 also helps endothelial cells stay stable. When NRP2 is lost, endothelial cells lose the junctional protein VE-cadherin, become more inflammatory and show increased adhesion molecules that can recruit immune cells.
The student will test how NRP2 controls endothelial barrier stability in human and mouse endothelial cells. They will study how cells respond to flow, inflammatory stimulation and lipid/nutrient stress, and will ask whether loss of VE-cadherin is the trigger that drives inflammatory activation. The project will also use an endothelial-specific mouse model to test whether NRP2 helps blood vessels adapt to dietary stress in vivo.

The student will receive broad interdisciplinary training in endothelial cell biology, receptor trafficking, live-cell and confocal imaging, flow assays, inflammatory signalling, monocyte adhesion, mouse genetics, vascular physiology, statistics and data interpretation. The project is suited to a student interested in cell biology, vascular biology, inflammation and mechanisms that preserve tissue health.
This is a mechanistic PhD project with strong preliminary data, clear aims and room for the student to shape the direction of the work.