Predominant Basal Directional Release of Thromboxane, but not Prostacyclin, by Placental Trophoblasts from Normal and Preeclamptic Pregnancies

Abstract

Objective-To investigate apical and basal releases of thromboxane (TX) and prostacyclin (PGI2) by trophoblasts (TCs) from normal and preeclamptic (PE) placentas.Methods-TCs isolated from normal and PE placentas were incubated in cell culture inserts for 48hrs. Medium from the upper (apical) and the lower (basal) chambers were then collected separately and measured for TX and PGI2 by their stable metabolites of TXB2 and 6-keto PGF1α by ELISA. Apical and basal releases of TX and PGI were also examined with apical exposure of TCs to arachidonic acid (AA)+/-aspirin at different concentrations. Villous tissue expressions for PGI synthase, TX synthase and TX (TP) receptor were examined by immunohistochemistry.Results-1) TXB2, but not 6-keto PGF1α, concentrations were significantly higher in the lower than in the upper chambers with both normal and PE TCs (p<0.01); 2) apical exposure of TCs to AA resulted in a significant increase in TX releases towards both the upper and the lower chambers in normal TCs (p<0.01), but only a significant increase in the upper chamber in PE TCs (p < 0.01); 3) aspirin could attenuate AA-induced TX release both in the upper and the lower chambers in normal, but not in PE, TCs (p<0.01), respectively; 4) there were no differences in 6-keto PGF1α productions both in normal and PE TCs treated with AA +/− aspirin; 5) intense staining of TX synthase and TP receptor was seen in syncytiotrophoblast layer, villous core vessels and stromal cells in preeclamptic placental tissue sections.Conclusion-Predominant basal release of TX together with intense staining of TX synthase and TP receptor in trophoblasts, stromal cells and villous core vessels are found in placentas from PE. We speculate if predominant basal release of TX by TCs occurs in vivo as we found in our in vitro culture condition, basal released TX may play a significant role in increased placental vasoconstriction such as in PE.

Changes in coagulation and hemodynamics during pregnancy: a prospective longitudinal study of 58 cases

“…Under the physiological conditions, TXB2 reflects activation of platelets. And TXB plays roles in some pathologic conditions induced by pregnancy [17,18]. In our study, plasma TXB2 level was increased in pregnancy.…”

Prevention of gravidic endothelial hypertension by aspirin treatment administered from the 8th week of gestation

“…22,30 A recent study on isolated trophoblasts showed that aspirin is able to decrease the release of thromboxane when the trophoblasts are isolated from normal but not from pre-eclamptic placentas. 31 This again could suggest that when the pathology is established, the beneficial effects of aspirin are absent.…”

Coagulation and prothrombotic state parameters: a clinical analysis during early pregnancy

“…If this occurs, thrombosis, fibrinoid necrosis, and atherosclerosis may be seen in the placenta and decidual vessels and can cause spontaneous abortion, preterm delivery, fetal distress, preeclampsia, and fetal growth restriction [10][11][12][13][14]. Studies of fetal growth restriction and preeclampsia performed with blood samples have reported an increase in TXB2 levels [15][16][17][18][19]. However, others believe that TXB2 does not change much during pregnancy [20].…”