The human placental anti-aggregating factor is neither prostacyclin, nor a prostacyclin metabolite |
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Authors: | MJ Dembl-Duchesne H Thaler-Dao C Chavis ACrastes de Paulet |
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Institution: | Institut National de la Santé et de la Recherche Médicale - U. 58 60, Rue de Navacelles - 34100 Montpellier, France |
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Abstract: | Using PGH2 as substrate, we have previously demonstrated that human placenta synthetizes mainly PGE2, TxB2 and PGD2(1,2). Other reports have shown that placental tissue generates a substance which inhibits ADP-induced platelet aggregation and which was supposed to be PGI2 (3). The present study indicates that the stability of that substance is different from the stability of prostacyclin (released by umbilical artery pieces). By GC-MS and multiple ion-monitoring, we have shown the presence of 6 keto-PGF1α (the stable metabolite of PGI2) in the umbilical artery incubation medium, while no trace of 6-keto-PGF1α could be found in the placental medium. No conversion of AA to 6-keto-PGF1α by placental microsomes was observed, even in the presence of antioxidants. The placenta possesses, in addition to the known 15-OH-PGDH and Δ-13 reductase activities, a weak 9 OH pGDH which is specific for PGF2α (and not PGI2 nor 6-keto-PGF1α). GC-MS analysis is showed that the expected metabolites of PGI2 through those three enzymes were not found in the placental medium, indicating that neither PGI2 synthesis nor metabolism could be demonstrated in the placenta. |
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Keywords: | AA arachidonic acid ADP adenosine diphosphate DTT dithiothreitol GSH reduced glutathione MID multiple ion detection NAD α-nicotinamide adenine dinucleotide PG prostaglandin PGDH prostaglandin dehydrogenase PRP platelet-rich plasma s d standard deviation |
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