Corticotrophin-releasing hormone (CRH) is produced by both the placenta and fetal membranes at term in man, and CRH mRNA has been detected in human placental tissue. The synthesis of CRH and its control during early pregnancy, however, have not been established, and the role of CRH produced in the placenta and fetal membranes is not known.
We examined whether amnion and placental tissue obtained between 12 and 15 weeks of gestation produced CRH in vitro, whether steroid modulation of output occurred and whether CRH affected prostaglandin (PG) output by the placenta and amnion.
Immunoreactive (ir) CRH output by amnion (2·8 ± 0·31 (s.e.m.) nmol/105 cells) was significantly (P<0·01) greater than that from placenta (1·76 ± 0·21 nmol/105 cells). Output of ir-CRH decreased in the presence of progesterone, but increased in the presence of cortisol and dexamethasone. There was no significant effect of progesterone or ir-CRH output by placental cells; however, ir-CRH output was increased in the presence of dexamethasone and cortisol. There was no significant effect of corticosterone on ir-CRH output by either amnion or placental cells. Both ACTH and CRH stimulated the output of PGE2 and PGF2α by amnion cells. In contrast, there was no significant effect of PGE2 output by placental cells maintained in the presence of either human CRH or ACTH. Output of PGF2α by placental cells was increased in the presence of both CRH and ACTH.
We conclude that both amnion and placental tissue produce CRH in early gestation, and that this output is modulated by steroids. CRH and ACTH stimulate PG output by amnion and placenta in early pregnancy, raising the possibility of local (autocrine and paracrine) interrelations in vivo.
Journal of Endocrinology (1990) 125, 153–159
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