Concentrations of activin A, inhibin A and follistatin in human amnion, choriodecidual and placental tissues at term and preterm

Abstract

To investigate labour-associated changes in production of activin and related hormones by gestational tissues we prepared extracts from amnion, choriodecidual and placental tissues delivered at term before labour (TNL; n=15), at term after spontaneous labour (TSL; n=15) or preterm (PTD; n=31) and measured concentrations of inhibin A, activin A and follistatin by ELISA. Activin concentrations in placental tissues were significantly (Mann-Whitney U-test; P<0·05) elevated with term labour (pg/mg protein, median; 1313 vs 2591), but in the PTD tissues concentrations were lower than those delivered spontaneously at term (3650 vs 2649). Inhibin concentrations also increased with term labour in the placenta (480 vs 686), but paradoxically decreased in amnion (188 vs 64) and choriodecidua (657 vs 358). Little or no significant changes in follistatin concentrations were observed. Concentrations of all three proteins were significantly correlated between amnion and choriodecidual tissues, and were significantly correlated with each other in most tissues (Spearman's ranked correlation; P<0·05). The activin:inhibin ratio in term amnion and choriodecidual tissues was increased 2 to 3-fold (P<0·0005 by MannWhitney U-test) after term labour, with similar trends also observed in the activin:follistatin ratio in placental tissue. These data suggest that a modest increase in placental activin and inhibin production may occur with labour at term. In addition, an increase in activin bioactivity may occur with labour, potentiating any paracrine effects of activin during parturition. The data, however, do not support an association between increased intrauterine activin biosynthesis and preterm delivery.

Secretion of inhibin A and inhibin B throughout pregnancy and the early postpartum period in chimpanzees

“…Using human explant tissue culture, it has been reported that inhibins A and B are secreted by the chorion laeve, whereas only inhibin A is secreted by the placenta. Furthermore, only low concentrations of both dimeric inhibins are secreted by the decidua parietalis and amnion (Riley et al 1996, Keelan et al 1999 and the mRNA for the subunits of inhibin A has been detected in human placenta (Petraglia et al 1987). It has been concluded that the placenta is a major source of circulating inhibin A in humans.…”

Activin A and activin receptors in gestational tissue from preeclamptic pregnancies

“…Of the three activins -A, B and AB -that have been identified in human tissues, activin A is the predominant form in pregnancy (Qu & Thomas 1995, Fowler et al 1998. The placenta and fetal membranes are the main sources of circulating activin A (Rabinovici et al 1992, Petraglia et al 1997, Keelan et al 1999. In early and mid pregnancy, maternal serum activin A levels are stable and low, rising dramatically from approximately 24 weeks of gestation, reaching peak levels proximate to term (Petraglia et al 1993a, Fowler et al 1998, Schneider-Kolsky et al 2000.…”

Imbalance of Amniotic Fluid Activin-A and Follistatin in Intraamniotic Infection, Inflammation, and Preterm Birth

“…Possible sources are fetal membranes and neutrophils with well-established roles on fighting infection (17,31). Our current data showed that intra-amniotic infection upregulated activin-A directly related to the level of AF inflammation.…”

“…We investigated AF samples from 168 women pregnant with singletons who had a clinically indicated amniocentesis to rule-out infection. Samples were retrieved by transabdominal amniocentesis for the purpose of i) second trimester genetic karyotyping [Gestational Age (GA), median [IQR range]: 19 [18 -20] weeks, n ϭ 19); ii) third trimester fetal lung maturity testing (GA: 36 [36 -37] weeks, n ϭ 20); iii) rule-out AF infection in women who had preterm labor contractions refractory to tocolysis, PPROM or advanced cervical dilatation (Ͼ3 cm) (GA: 28 [25][26][27][28][29][30][31] weeks, n ϭ 129). Ruleout AF infection cases were further grouped by timing of birth (term or preterm), membrane status at amniocentesis (intact membranes or PPROM) and microbiologic culture results of the AF (positive or negative).…”