Predominant basal directional release of thromboxane, but not prostacyclin, by placental trophoblasts from normal and preeclamptic pregnancies.
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 48h. 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 PGF1alpha 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 PGF1alpha, 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 release 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 PGF1alpha 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.


CONCLUSIONS
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.
Zhao
S
S
Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Gu
Y
Y
Lewis
D F
DF
Wang
Y
Y
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000328:Adult; D016718:Arachidonic Acid / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D011464:Epoprostenol / Q000378:metabolism*; D005260:Female; D006801:Humans; D010920:Placenta / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D011225:Pre-Eclampsia / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy; D017482:Receptors, Thromboxane / Q000032:analysis / Q000378:metabolism; D013929:Thromboxane B2 / Q000032:analysis; D013930:Thromboxane-A Synthase / Q000032:analysis; D013931:Thromboxanes / Q000032:analysis / Q000378:metabolism*; D014327:Trophoblasts / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D014661:Vasoconstriction
D017482:Receptors, Thromboxane; D013931:Thromboxanes; D016718:Arachidonic Acid; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D013930:Thromboxane-A Synthase; D001241:Aspirin