Endothelial cell expression of monocyte chemotactic protein-1, tissue factor, and thrombomodulin on hydrophilic plasma polymers.

Endothelial cells (EC) from human aortas, microvessels, and pulmonary arteries were examined for their expression and activity of monocyte chemotactic protein-1 (MCP-1), tissue factor, and thrombomodulin in response to tumor necrosis factor-alpha (TNFalpha) on the hydrophilic plasma polymers gamma-butyrolactone (GBL) and N-vinyl-2-pyrrolidone (NVP), along with a fibronectin (FN) control. RNAs isolated from EC grown on these substrates were subjected to reverse transcription-polymerase chain reaction (RT-PCR) and dot-blot analysis. EC expression of MCP-1 and tissue factor was very low in the absence of TNFalpha but high for constitutively expressed thrombomodulin. TNFalpha induced EC expression and activity of MCP-1 and tissue factor and suppressed that of thrombomodulin on all substrates. Greater differences were seen with regard to cell origin, but little difference was seen among substrates. Basal secretion of MCP-1 was very low in aortic and pulmonary artery EC and even less in microvascular EC. TNFalpha increased MCP-1 secretion significantly in aortic and pulmonary artery EC but to a lesser extent in microvascular EC. In contrast, tissue factor expression was greater in pulmonary artery EC compared to microvascular and aortic EC. Basal expression of thrombomodulin was largely comparable for all three cell types grown on different surfaces, but TNFalpha suppressed thrombomodulin to different extents depending on the origin of the EC. The activity of tissue factor and thrombomodulin and the secretion of MCP-1 by EC were largely correlated with the expression of these genes. We conclude that EC origin may be an important determinant of cellular function on hydrophilic plasma polymer substrates. However, the differences in cellular function due to variations in substrate surface hydrophilicity could have been masked by the extracellular matrix remodeling that presumably occurred during EC growth to confluence.