Kroos M J, Starreveld J S, Verrijt C E, van Eijk H G, van Dijk J P
Department of Chemical Pathology, Erasmus University Rotterdam, The Netherlands.
Eur J Obstet Gynecol Reprod Biol. 1996 Apr;65(2):231-4. doi: 10.1016/0301-2115(95)02368-2.
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 (FAC) 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.
本研究的目的是检测合体滋养层细胞响应母体铁供应调节时调控转铁蛋白受体（TfR）合成的能力。所用模型为原代滋养层细胞培养。从足月人胎盘中分离的滋养层细胞在缺铁（199培养基）、铁耗尽（去铁胺（DFO））和铁补充（二价铁转铁蛋白（hTf-2Fe）、柠檬酸铁铵（FAC）培养基）条件下培养。补充hTf-2Fe会导致TfR合成减少。FAC不会调节TfR合成。DFO导致的铁剥夺明显刺激了TfR合成。这些结果表明，分化中的滋养层细胞通过调整TfR合成速率来响应（转铁蛋白介导的）铁供应的扰动。以培养中的合体滋养层细胞作为体内母体/胎儿界面的模型，我们的结果表明胎盘能够对铁摄取能力进行短期调节。
