Objective: The objectives of this study were to investigate the effect of activin A and follistatin on firsttrimester cytotrophoblast invasion in culture and to study the secretion of inhibin A, activin A and follistatin by these cells in vitro. Design and methods: Cytotrophoblasts were isolated from human placental chorionic villous tissue obtained from 6-8, 8-10 and 10 -12 weeks gestation. Cells were cultured for 3 days on cell-culture inserts coated with gelatine for invasion studies and in 24-well culture plates for secretion studies. The effects of activin A (10 ng/ml), follistatin (100 ng/ml), interleukin 1b (IL-1b; 10 ng/ml) and epidermal growth factor (EGF; 10 ng/ml) on cytotrophoblast invasion were investigated using a nonradioactive invasion assay. Secretion of inhibin A, activin A and follistatin in the presence of EGF, IL-1b, activin A and follistatin were measured using in-house ELISAs. Results and conclusion: Activin A, follistatin and EGF had a significant stimulatory effect on cytotrophoblast invasion from 6-10 weeks gestation. IL-1b had a significant stimulatory effect at 8 -10 weeks and a significant inhibitory effect on invasion at 10-12 weeks gestation. Follistatin also had a significant inhibitory effect on invasion at 10-12 weeks gestation. In the secretion study, activin A secretion at 8-10 weeks was significantly stimulated by IL-1b and EGF. At 10 -12 weeks, follistatin and EGF had a significant inhibitory effect on activin A secretion. Follistatin secretion was significantly increased in the presence of IL-1b at 6-8 weeks gestation. Inhibin A secretion was not significantly altered by EGF, IL-1b, activin A and follistatin. These results show that activin A promotes invasion of first-trimester cytotrophoblasts until 10 weeks gestation. There is a difference in the control of secretion of these proteins dependent on the gestation, suggesting that there is a tight regulation in the function of first-trimester trophoblasts depending on the gestational age.European Journal of Endocrinology 152 909-916
Maternal circulating levels of inhibin A are significantly lower in patients with clinical symptoms of miscarriage. The objective of this study was to quantify relative expression of inhibin alpha, inhibin/activin betaA, betaB, betaC, follistatin, activin receptors and beta-glycan genes and content of inhibin A, activin A and follistatin protein in villous tissue of first trimester miscarriages and gestation-matched normal pregnancies. Twelve women with clinical symptoms of miscarriage were matched with 12 normal pregnancies for gestational age. Total RNA was isolated from placental samples. Complementary DNA produced by reverse transcription was used in the real-time PCR to quantify the expression of the genes. The ratio between the target and rRNA 18S was calculated to provide relative gene expression. Villous tissue homogenates were used for the determination of the content of inhibin A, activin A and follistatin protein. Maternal serum was assayed for inhibin A, activin A and follistatin. All villous samples expressed inhibin alpha, inhibin/activin betaA, betaB, betaC, follistatin, activin receptors (ACTRIA, ACTRIB, ACTRIIA, ACTRIIB) and beta-glycan genes. There was no significant difference in the relative expression of these genes between the groups. Villous content of inhibin A, activin A and follistatin were also not different between the two groups. Maternal serum levels of inhibin A were significantly lower in the miscarriage group compared to the controls. The decreased maternal levels of inhibin A in miscarriage patients could be due to a decrease in placental mass prior to embryonic demise. This finding also confirms that the trophoblast is the major source of inhibin A after the luteo-placental shift in early pregnancy.
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