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Defect of Villous Cytotrophoblast Differentiation into Syncytiotrophoblast in Down's Syndrome

2000; Oxford University Press; Volume: 85; Issue: 10 Linguagem: Inglês

10.1210/jc.85.10.3700

1945-7197

Jean‐Louis Frendo,

Trauma and Emergency Care Studies

The syncytiotrophoblast (ST) is one of the major components of the human placenta as it is involved in feto-maternal exchanges and the secretion of pregnancy-specific hormones.The aim of this study was to elucidate the formation and function of the ST in trisomy 21 (Down syndrome).We first used the in vitro model of cytotrophoblast differentiation into ST.Cytotrophoblasts were isolated from 15 trisomy 21-affected placentas (12-35 weeks of gestation) and 10 gestational age-matched control placentas.In vitro cytotrophoblasts isolated from normal placenta fused to form the ST.This was associated with an increase in the transcript levels and the secretion of human chorionic gonadotropin (hCG), human placental lactogen (hPL), placental growth hormone (PGH) and leptin.In trisomy 21-affected placentas, we observed a defect (or a delay) in ST formation and a dramatic decrease in the synthesis and secretion of these hormones as compared to cultured cells isolated from control age-matched placentas.These results were confirmed by a significant (p<0.001)decrease in gene expression in total homogenates of trisomy 21-affected placentas as compared to control.These results will be of help in understanding the maternal hormonal markers of fetal trisomy 21 and the consequences of placental defects for fetal development.