Defect of syncytiotrophoblast formation and human chorionic gonadotropin expression in Down's syndrome

Citation
N. Massin et al., Defect of syncytiotrophoblast formation and human chorionic gonadotropin expression in Down's syndrome, PLACENTA, 22, 2001, pp. S93-S97
Citations number
24
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
PLACENTA
ISSN journal
01434004 → ACNP
Volume
22
Year of publication
2001
Supplement
A
Pages
S93 - S97
Database
ISI
SICI code
0143-4004(200104)22:<S93:DOSFAH>2.0.ZU;2-X
Abstract
The syncytiotrophoblast (ST) is a major component of the human placenta as it is involved in fete-maternal exchanges and the secretion of pregnancy-sp ecific hormones. We have studied the formation and function of the ST in no rmal and trisomy 21 (T21)-affected placenta using the in vitro model of cyt otrophoblast differentiation into ST. Cytotrophoblast cells were isolated f rom first trimester, second trimester and term placentae. In vitro cytotrop hoblast cells isolated from normal placenta fused to form the ST. This was associated with an increase in the transcript levels and the secretion of h uman chorionic gonadotropin (hCG). However, the secretion of hCG decreased through pregnancy. In T21-affected placentae, we observed a defect (or a de lay) in ST formation and a dramatic decrease in the synthesis and secretion of this hormone compared with cultured cells isolated from control age-mat ched placentae. These results sere confirmed by a significant (P<0.05) decr ease in transcript levels of <alpha> and beta subunits of hCG in total homo genates of T21-affected placentae compared with controls. These results sug gest a decrease in functional mass of ST in T21 placenta, and therefore a d ecrease in production of placental pregnancy-specific polypeptide hormones. (C) 2001 IFPA and Harcourt Publishers Ltd.