Abstract

Experiments were performed to determine the ability of isolated cells from human amnion, chorion, and decidua to hydrolyze estrone sulfate (E1S) to free estrone (E1) and estradiol (E2). Tissues were obtained from eight women after spontaneous onset of labor and vaginal delivery and from eight women undergoing elective cesarean section at term before the onset of labor. The tissues were obtained immediately after delivery, dispersed into isolated cell preparations using 0.05% collagenase, and incubated in Krebs-Ringer bicarbonate at 37 degrees C for 4 h. E1 and E1S were measured by specific RIAs. All three tissues from both patient groups produced E1 and E2 in a dose-dependent fashion from the E1S precursor. In both patient groups, chorion and decidua cells produced significantly more E1 and E2 than amnion cells. The chorion cells from the spontaneous labor group produced significantly more E1 than chorion cells from the cesarean section group. The chorion and decidua cells from the spontaneous labor group produced significantly more E2 than corresponding cells from the cesarean section group. The hydrolysis of E1S to E1 and E2 was significantly inhibited in a dose-dependent fashion by increasing concentrations of oxytocin and (Bu)2cAMP. Dispersed cells from amnion, chorion, and decidua also converted [3H]E1S to radiochemically pure [3H]E1. Chorion and decidua cells were significantly more active in this respect than amnion. The presence of excessive amounts of dehydroepiandrosterone sulfate (DHAS) did not significantly alter this reaction. All three tissues also hydrolyzed [3H]dehydroepiandrosterone sulfate, but in chorion and decidua, this activity was significantly less than the hydrolysis of [3H]E1S. We conclude that human amnion, chorion, and decidua possess the capability to hydrolyze E1S to free estrogen and that this activity in chorion and decidua is increased after spontaneous vaginal delivery. It is possible that this activity and its regulation are important factors in the local synthesis of free estrogen, which, in turn, may influence myometrial contractility.

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