Molecular Human Reproduction, Vol. 6, No. 1, 5-10,
January 2000
© 2000 European Society of Human Reproduction and Embryology
Genetic diagnosis |
HCG concentration and receptor gene expression in placental tissue from trisomy 18 and 21
1 Academic Departments of Obstetrics and Gynaecology, Royal Free and University College Medical School, London, UK, 2 Laboratory of Molecular Biology and Medicine, Department of Obstetrics and Gynaecology, University of Louisville, Louisville, USA, and 3 The Research Laboratory on Reproduction, Free University of Brussels School of Medicine, Brussels, Belgium
Abstract
Trisomy 21 is associated with high maternal serum concentrations of intact human chorionic gonadotrophin 
(HCG) and free ß-HCG whereas these concentrations are markedly decreased in trisomy 18. In this study, we investigated the effect of trisomy 21 and 18 on endogenous HCG concentrations and luteinizing hormone (LH)/HCG receptor expression in placental villous tissue in eight trisomy 21, six trisomy 18 and 42 chromosomally normal samples, collected at 12–16 weeks gestation. The tissue concentrations of intact HCG, free -HCG and free ß-HCG subunits were measured using solid-phase two-site immunoradiometric assay. LH/HCG receptor expression was evaluated with immunohistochemistry and in-situ hybridization. Villous tissue in trisomy 21 contained higher ß-HCG concentrations than the controls (P < 0.05). In trisomy 18 cases, the ß-HCG concentration was lower than in the control group (P < 0.01). Both immunocytochemistry and in-situ hybridization demonstrated a more intense staining of the trophoblast in cases of trisomy 21 and 18, compared with controls with the strongest signal in cases of trisomy 18 (P < 0.01). We concluded that in trisomy 21 the high tissue HCG concentration and expression of LH/HCG receptor in the trophoblast may reflect the relative immaturity of the trophoblastic tissue whereas in trisomy 18, the very low concentration of endogenous HCG, associated with an over-expression of LH/HCG receptor in the trophoblast, is probably secondary to the poor differentiation of the cytotrophoblast.
HCG/placenta/pregnancy/receptors/trisomy
Notes
4 To whom correspondence should be addressed at: Academic Department of Obstetrics and Gynaecology, University College London Medical School, 86–96 Chenies Mews, London WC1E 6HX, UK
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