Effects of platelets from men with risk factors for atherosclerosis on endothelial cell proliferation and prostacyclin production in vitro

Abstract

The hypothesis that variations in platelet size or composition might affect some endothelial cell (EC) functions was tested. Large and small platelets stimulated cell proliferation and prostacyclin production to the same extent at the same amount of protein. Endothelial cells exposed to platelet factors from healthy men at statistically high risk of cardiovascular disease (n = 30) manifested significantly less DNA synthesis than did EC exposed to platelet factors from men at statistically low risk (n = 30) (p = 0.007). There was no difference in prostacyclin production between the groups. Nor were there any differences in EC or smooth muscle cell (SMC) proliferation or in prostacyclin production between cells exposed to platelet factors from smokers and those exposed to platelet factors from non-smokers. In stepwise regression of the results for high risk groups, with thymidine incorporation as the dependent variable, including diastolic blood pressure, s-triglycerides and s-cholesterol, s-triglycerides were inversely correlated to thymidine incorporation. We suggest that the decreased endothelial cell DNA synthesis after exposure to platelet factors from high risk individuals may imply a decreased capability for damage repair in the vascular wall, and that the differences in platelet effects on EC proliferation may be due to differences in lipids, especially triglycerides.

Key Words:

• platelets
• risk factors
• atherosclerosis
• endothelium
• proliferation
• prostacyclin