Selective effects of preeclamptic sera on human endothelial cell procoagulant protein expression.

Current concepts of preeclampsia suggest that dysfunction of maternal vascular endothelium in vivo is a central pathogenetic feature of this syndrome. This hypothesis is suggested by the activation of the coagulation cascade associated with preeclampsia and evidence for a role of endothelium in maintaining thromboresistance. Previous in vitro studies with monolayers of human umbilical vein endothelial cells demonstrated direct cytotoxic effects of sera from preeclamptic parturients. In the current studies, we have examined the in vitro expression of three procoagulant protein activities regulated by endothelial cells: cellular fibronectin, an important mediator of platelet aggregation known to be elevated in preeclamptic women in vivo; tissue factor, the most potent endogenous procoagulant activity; and von Willebrand factor, a major component of coagulation factor VIII. Monolayer cultures of human umbilical vein endothelial cells were incubated with pregnancy sera for 24 hours before these proteins and activities were quantified. Exposure of identical endothelial cell cultures to predelivery preeclamptic sera caused significantly greater release of cellular fibronectin than postdelivery preeclamptic or predelivery or postdelivery normal pregnancy sera (p less than 0.05). However, neither tissue factor activity nor von Willebrand factor expression appeared to be increased preferentially by preeclamptic sera. The data indicate that sera from women with preeclampsia induce a selective, but not a generalized, activation of endothelial cell procoagulant protein production.