VEGF-E enhances endothelialization and inhibits thrombus formation on polymeric surfaces

Thrombotic complications of long-terra blood-contacting devices can be avoided by formation of an endothelial cell layer on the blood-contacting surface. The endothelial cells form a bioactive boundary between the synthetic surface and blood, regulating ha haemostasis and inflammation. Biofunctionalization of synthetic blood-collecting surfaces is necessary to accommodate growth of endothelial cells. Vascular endothelial growth factor E (VEGF-F) or collagen I may stimulate endothelialization of a polymeric surface coating of a prototype small diameter vascular prosthesis. VEGF-E was produced hi Escherichia coli and could be easily purified in large quantities. Recombinant VEGF-E or purified collagen I was allowed to adsorb onto the polymeric surfaces and enhanced formation of an endothelial cell layer. Adsorption of VEGF-E was increased by the inclusion Of the anti-coagulant drug heparin in the polymeric coating. Collagen I adsorption induced rapid thrombin generation and increased platelet adhesion of surfaces with or without heparin. VEGF-E a( inhibited thrombus formation, and did not interfere with the anti-thrombogemic effect of heparin). Additionally, VEGF-E did not affect platelet adhesion. Adsorption of VEGF-E, especially on heparin containing surfaces, provides an economical strategy to improve endothelialization of cardiovascular implants without disturbing blood-compatibility.