Secretion of prostaglandins and endothelin-1 by decidual endothelial cells from normal and preeclamptic pregnancies: Comparison with human umbilical vein endothelial cells

OBJECTIVE: An increasing amount of circumstantial evidence points to the maternal endothelial cell as centrally involved in the syndrome of preeclampsia. The purposes of this study were (1) to compare the secretion of vasoactive substances by maternal decidual endothelial cells with that of umbilical vein endothelial cells, widely used as a surrogate for endothelial cells in general, and (2) to compare secretion of the same vasoactive substances by decidual endothelial cells from normal and preeclamptic pregnancies. STUDY DESIGN: Endothelial cells were isolated from umbilical veins and from decidual biopsy specimens collected at cesarean section delivery from both normal and preeclamptic women. Cells were maintained in culture until passage 2, when secretion by the three endothelial cell populations of the vasodilators prostaglandin E 2 and prostacyclin and the vasoconstrictor endothein-1 was examined. In Addition to control incubations, their responses to stimulation and suppression of secretion were compared. RESULTS: In control incubations normal decidual endothelial cells secreted lower amounts of prostacyclin, prostaglandin E 2, and endothelin than did human umbilical vein endothelial cells. All cell types had qualitatively similar responses to the stimuli used, but quantitatively different responses were noted between human umbilical vein endothelial cells and normal decidual endothelial cells for all metabolites human umbilical vein endothelial cells and normal decidual endothelial cells for all metabolites examined. Preeclamptic decidual endothelial cells secreted significantly more prostaglandin E 2 thandid normal decidual endotelial cells in response to stimulation. CONCLUSIONS: We have delineated levels of secretion of vasoactive substances by human late pregnancy decidual endothelial cells and their responses to manipulation of secretory pathways. There are widely used as a surrogate for maternal endothelial cells). The differences between normal and preeclamptic decidual endothelial cells in prostaglandin E 2 secretion may point to altered regulation of arachidonic acid metabolic pathways in preeclampsia.