Abstract
Small‐diameter vascular grafts rapidly fail as a result of blood coagulation and platelet deposition. Endothelial cells lining the inner side of blood vessels can provide the graft lumen with an antithrombogenic surface. One of the remaining problems is cell detachment after restoration of blood flow, because of infiltration of leukocytes that respond to an inflammatory‐like activation of the endothelial cells. This endothelial activation is possibly caused by the surface characteristics of the underlying polymer. To get more insight into the effects of the polymer surface on endothelial cell activation, we seeded human umbilical vein endothelial cells (HUVECs) in various densities and subsequently grew them on tissue culture polystyrene (TCPS; hydrophilic) and polystyrene (PS; hydrophobic) surfaces. To improve cell adhesion, surfaces were coated with purified fibronectin prior to cell seeding. During proliferation, the expressions of the leukocyte adhesion molecules ICAM‐1 and VCAM‐1 were determined. Results indicate that ICAM‐1 expression is not influenced by the character of the polymer surface, and that VCAM‐1 expression is slightly higher on the TCPS surface. Expressions of both adhesion molecules are influenced by the seeding density and time of proliferation. At low seeding densities (≤ 10,000 cells/cm^2^), a relatively low percentage of nonexogenously activated cells expressed ICAM‐1 during the first 3 days of proliferation compared to higher seeding densities. Although less pronounced, this was also observed for the percentage of cells expressing VCAM‐1. During proliferation, the amount of ICAM‐1 per endothelial cell increased, whereas the expression of VCAM‐1 remained low. The absence of large differences in leukocyte adhesion molecule expression by endothelial cells grown on TCPS or PS is possibly caused by coating of the surfaces with fibronectin. It is known that surface hydrophilicity influences protein adsorption. Although this had no or little effect on leukocyte adhesion molecule expression, endothelial cell growth was affected, because proliferation was slower on the hydrophobic PS. © 2003 Wiley Periodicals Inc. J Biomed Mater Res 65A: 51–59, 2003