The aim of this study was to examine the capacity of the syncytiotrophoblast to regulate transferrin receptor (TfR) synthesis in response to modulations in maternal iron supply. The model used was the primary trophoblast cell culture. Trophoblast cells isolated from term human placentas were cultured in iron-poor (Medium 199), iron-depleted (desferrioxamine (DFO)) and iron supplemented (diferric transferrin (hTf-2Fe), ferric ammonium citrate (FAG)) medium. TfR synthesis was reduced in response to hTf-2Fe supplementation. FAC did not modulate TfR synthesis. Iron deprivation by DFO resulted in clear stimulation of TfR synthesis. These results show that the differentiating trophoblast cells respond to pertubations in the (transferrin-mediated) iron supply by adjustments in the rate of TfR synthesis. Taking syncytiotrophoblast in culture as model for the maternal/fetal interface in vivo, our results would suggest that the placenta is able to make short term adjustments of the capacity for iron uptake.

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European Journal of Obstetrics & Gynecology and Reproductive Biology
Department of Clinical Chemistry

Kroos, M.J, Starreveld, J.S, Verrijt, C.E.H, van Eijk, H.G, & van Dijk, J.P. (1996). Regulation of transferrin receptor synthesis by human cytotrophoblast cells in culture. European Journal of Obstetrics & Gynecology and Reproductive Biology, 65(2), 231–234. doi:10.1016/0301-2115(95)02368-2