Background

Cell migration is a fundamental event in a variety of biological processes, including the inflammatory response by the organism to repair damages from bacteria, viruses or other injuries, and the formation of new blood vessels (neo-angiogenesis). Proteolytic enzymes degrade the endothelial basement membrane and the extra-cellular matrix (ECM), thus allowing endothelial cells to migrate through lysed matrix proteins. One of the main orchestrators of the whole process is the system formed by uPA (urokinase-plasminogen activator) and its receptor uPAR (Blasi & Carmeliet, 2002). While regulating extracellular proteolysis, the uPA/uPAR system activates a number of intracellular signaling pathways, ultimately enabling inflammation and angiogenesis to occur (Smith & Marshall, 2010). In healthy individuals, the production and activity of uPA/uPAR and its inhibitor are finely balanced; conversely, when dysregulated, uPA/uPAR may decisively contribute to the onset of many pathologic conditions.