Choriodecidual adhesion promotes decidual prolactin transport by human fetal membrane.

The theory of human decidualized endometrium to produce prolactin (PRL) throughout gestation has led to the implication that such production is related to the source of amniotic fluid PRL (afPRL). This study confirms that fetal membranes, amnion and amniochorion with or without adherent decidua, are unable to transfer significant quantities of exogenously administered PRL from the maternal to fetal compartments in vitro. Incubation of amniochorion with decidua adherent to chorion results in a significant increase in the amount of endogenous PRL appearing on the fetal side of the membrane concomitant with a rise in decidual PRL on the maternal side. The results suggest that transport of decidual PRL to amniotic fluid is predicated on retention of the cellular adhesion between maternal decidua and fetal chorion as exists in vivo. Disruption of decidual contact with fetal membrane results in failure of PRL transport to the fetal side despite a steady accumulation of PRL on the maternal side. We conclude that human fetal membranes are highly permeable to decidual PRL in vivo, and that decidua probably represents the major source of afPRL.