Some new prospects in the mechanism of control of arachidonate metabolism in human placenta and amnion |
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Authors: | MJ Dembl-Duchesne H Thaler-Dao C Chavis A Crastes de Paulet |
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Institution: | Institut National de la Santé et de la Recherche Médicale - U.58 60, Rue de Navacelles - 34100 - Montpelleir, France |
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Abstract: | The conversion of (1-14C) PGH2 was studied in human placental and fetal membrane cellular preparations (tissue fragments, homogenate, cytosol, microsomes). Placental and amnion homogenates convert labelled PGH2 into PGE2 through a very active PGE2 isomerase. However isolated placental microsomes do not metabolise PGH2 into PGE2 but into T×A2 (identified as T×B2 by GC-MS) and presumably 12-HHT. This microsomal T×A2 synthetase is not active in the whole tissue nor in the homogenate. Placental cytosol gives mainly PGD2. No conversion into PGI2 (identofied as 6 keto PGF1α) nor PGF2α was observed in any fraction.Some aspects of PG synthesis regulation by the placental cytosol were studied: the cytosol contains a heat-stable factor that inhibits T×A2 synthesis and shifts PGH2 placental microsome metabolism towards PGE2. In addition the placental cytosol inhibits human platelet-aggregation through a heat-labile factor which is not PGI2 nor PGD2. A multiple step regulation of the various PG metabolites synthetised from arachidonic acid in the placenta can be outlined and its physiological implications are discussed. |
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Keywords: | MNNG N-methl-N′-vitro-N-nitroso quanidine BSTFA N-O-bis-trimethyl silyl trifluoroacetamide p-CMB p-chloromercuribenzoic acid ADP adenosine diphosphate BSV bull seminal vesicle PRP platelet-rich plasma PPP platelet-poor plasma OH-FA hydroxy fatty acids |
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