Prolactin release from perifused human decidual explants; effects of decidual prolactin-releasing factor (PRL-RF) and prolactin release-inhibitory factor (PRL-IF)

Abstract

The dynamics of prolactin release from human decidual explants were studied under basal conditions, in response to decidual prolactin-releasing factor (PRL-RF), and in response to PRL-RF in the presence of decidual prolactin release-inhibitory factor (PRL-IF) or other factors known to inhibit prolactin release in static cultures. Explants were persfused with medium at a rate of 6 ml/h, and the medium was collected at 5 min intervals. The Eplants released prolactin for up to 20 h without evidence of cell necrosis, with the rate of prolactin decreasing gradually from 3.9 ± 0.1 ng/5 min during the first 2 h to 2.2 ± 0.1 ng/5 min during the last 2 h of exposure. PRL-RF, a 23.5 K Mr protein released by the placenta, stimulated a dose-dependent increase in prolactin release from the persfused explants that occurred within the first 5 min of exposure and persisted until the exposure to the releasing factor was discontinued. PRL-IF a 35–45 K M r protein released by the decidua, caused a dose-dependent inhibition of PRL-RF-mediated prolactin release. Dibutyryl cAMP, cholera toxin, sn-1, 2-dioctonylglycerol, PMA, and arachidonic acid, which inhibit basal prolactin release from static decidual cultures, also caused a dose-dependent inhibition of prolactin release in response to PRL-RF. In each instance, the maximal dose of the agents tested inhibited PRL-RF-mediated prolactin release by greater than 84 per cent. These results indicate that the stimulation of prolactin by PRL-RF is inhibited by PRL-IF and pharmacologic agents that inhibit basal prolactin release. The inhibition of PRL-RF-mediated prolactin release by PRL-IF strongly suggests that the decidua may modulate its own responsiveness to secretogogues by an autocrine/paracrine mechanism.