Iron transport in pregnancy is an active one-way process, from mother to fetus. Early in gestation fetal iron needs are low, and so is trans-placental transport, but as erythropoiesis develops, rising fetal iron needs are met by trans-placental iron transport. Apparently, the fetus is protected against iron toxicity as well as against iron deficiency, the latter even if maternal iron stores are depleted. Fetectomy experiments in animals indicate that placental iron uptake is an autonomous process, independent of the presence of a fetus. The narrow and, in the course of pregnancy, enonnously changing difference between iron deficiency and iron toxicity strongly suggests that maternal-fetal iron transport needs to be regulated. This thesis deals with some aspects of the regulation of placental iron uptake. Cllapter 3 describes the development of a cell culture model to study placental iron uptake. Cllapter 4 deals with characteristics of transferrin receptors in these cells and chapter 5 describes the regulation of transferrin receptor expression in nonnal hmnan term trophoblast cells in vitro. Finally, chapter 6 describes pregnancy-related changes of maternal transferrin, the iron donor for the placenta. In this chapter an animal model is used, the guinea-pig.

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Erasmus University Rotterdam
H.G. van Eijk (Henk)
hdl.handle.net/1765/50914
Erasmus MC: University Medical Center Rotterdam

Bierings, M. (1989, December 6). Placental iron uptake and its regulation. Retrieved from http://hdl.handle.net/1765/50914