ArticlePlacenta2008
Predominant basal directional release of thromboxane, but not prostacyclin, by placental trophoblasts from normal and preeclamptic pregnancies.
Article in Placenta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Endothelial Impairment in HIV-Associated Preeclampsia: Roles of Asymmetric Dimethylarginine and Prostacyclin.International journal of molecular sciences · 2025Article
- Extracellular Vesicles and Preeclampsia: Current Knowledge and Future Research Directions.Sub-cellular biochemistry · 2021Review
- Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020Review
- Molecular Targets of Aspirin and Prevention of Preeclampsia and Their Potential Association with Circulating Extracellular Vesicles during Pregnancy.International journal of molecular sciences · 2019Review
- Molecular determinants of microvascular dysfunction in hypertensive pregnancy and preeclampsia.Microcirculation (New York, N.Y. : 1994) · 2018Article
- An advanced human in vitro co-culture model for translocation studies across the placental barrier.Scientific reports · 2018Article
- Thrombosis recanalization by paeoniflorin through the upregulation of urokinase‑type plasminogen activator via the MAPK signaling pathway.Molecular medicine reports · 2016Article
- Lack of Thromboxane Synthase Prevents Hypertension and Fetal Growth Restriction after High Salt Treatment during Pregnancy.PloS one · 2016Article
- Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia.Advances in pharmacology (San Diego, Calif.) · 2016Article
- Bioactive factors in uteroplacental and systemic circulation link placental ischemia to generalized vascular dysfunction in hypertensive pregnancy and preeclampsia.Biochemical pharmacology · 2015Review
- Genetic, immune and vasoactive factors in the vascular dysfunction associated with hypertension in pregnancy.Expert opinion on therapeutic targets · 2015Review
- Coagulation and prothrombotic state parameters: a clinical analysis during early pregnancy.Irish journal of medical science · 2011Article
- Amniotic fluid eicosanoids in preterm and term births: effects of risk factors for spontaneous preterm labor.Obstetrics and gynecology · 2011Article
- D2-40/podoplanin expression in the human placenta.Placenta · 2011Article
- Molecular and vascular targets in the pathogenesis and management of the hypertension associated with preeclampsia.Cardiovascular & hematological agents in medicinal chemistry · 2010Article
- Proteases and sFlt-1 release in the human placenta.Placenta · 2010Article
- Decreased nephrin and GLEPP-1, but increased VEGF, Flt-1, and nitrotyrosine, expressions in kidney tissue sections from women with preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2009Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate apical and basal releases of thromboxane (TX) and prostacyclin (PGI2) by trophoblasts (TCs) from normal and preeclamptic (PE) placentas.
methodsTCs 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.
conclusionPredominant 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.
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