Mol. Hum. Reprod. Advance Access published online on September 10, 2004
Molecular Human Reproduction, doi:10.1093/molehr/gah110
© 2004 by Oxford University Press
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1 Department of Obstetrics and Gynaecology, Royal Free University College Medical School, 86-96 Chenies Mews, London WC1E 6HX, UK
* To whom correspondence should be addressed. E-mail: s.muttukrishna{at}ucl.ac.uk.
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
Accepted August 20, 2004
Article
Inhibin, activin, follistatin, activin receptors and
-glycan gene expression in the villous tissue of miscarriage patients
Abstract 
, inhibin/activin 
A, B, C, follistatin, activin receptors and -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 , inhibin/activin A, B, C, follistatin, activin receptors (ACTRIA, ACTRIB, ACTRIIA, ACTRIIB) and -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.-glycan; follistatin; inhibin.
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