The Effect of Vitronectin and Other Extracellular Matrix Molecules on Endothelial Expansion and Plasminogen Activation

Endothelial recovery following procedures used to alleviate blood vessel occlusion is modulated by the local extracellular matrix upon which it has to migrate and proliferate. This extracellular material is derived from vessel wall cells, and plasma proteins which bind to the exposed surfaces. We have demonstrated that vitronectin adsorbs efficiently to tissue culture polystyrene in competition with other plasma proteins, which suggests that it may adsorb to biomaterial surfaces in vivo. We have compared the adhesion, migration and proliferation of human umbilical artery endothelial cells on surface-coated vitronectin, with other extracellular matrix molecules encountered in this environment, namely fibronectin, laminin and collagen types I and IV. Endothelial proliferation was significantly reduced on the vitronectin surface. This was correlated with an increase in the ratio of plasminogen inhibitor-! to urokinase in the cell/matrix layer. Laminin coated surfaces limited increases in endothelial culture area, due to poorer cell spreading on this surface. Such combination of cellular responses to vitronectin and laminin would discourage endothelial recovery, and encourage smooth muscle hyperplasia in vivo. These considerations are important in the design of biomaterial surfaces to optimise endothelial recovery