Elucidating Mechanisms of Genetic Cross-Disease Associations at the PROCR Vascular Disease Locus

Using genetic analysis, human recall-by-genotype and in vitro experimentation, researchers demonstrated that PROCR-219Gly increased plasma levels of (activated) protein C through endothelial protein C receptor ectodomain shedding in endothelial cells, attenuating leukocyte–endothelial cell adhesion and vascular inflammation.