HORMONAL REGULATION OF IODIDE UPTAKE IN PLACENTAL PRIMARY CULTURES

1UCD Conway Institute, UCD, Belfield, Dublin, Ireland, 2National Maternity Hospital, Dublin, Ireland

Abstract

Maintenance of adequate iodine supply to the developing fetus is dependent not only on maternal dietary iodine intake but also active placental iodide transport. The sodium iodide symporter (NIS) gene and protein have been identified in human placental trophoblasts and indeed have been shown to have a role in iodide accumulation by the placenta.
The objectives of this study were to examine the effects of different pregnancy associated hormones on the uptake of iodide by the placenta. Placentas were obtained from women undergoing elective caesarean section, physically and enzymatically dispersed, and a primary culture of placental trophoblast cells separated by centrifugation and purified by immunomagnetic separation. Optimum 125I incubation times were established experimentally. 125I uptake by trophoblast cells peaked between 6 and 9 hours. Pre-incubation with various hormones (Estradiol, Prolactin, Oxytocin, Human Chorionic gonadotrophin (hCG) and progesterone) was performed over 12 hours and 125I uptake measured after 6 hours. Uptakes were performed in the presence and absence of potassium perchlorate (100µM) and measured in cpm 125I accumulated by cells. Uptake of 125I could be diminished by 66% in the presence of potassium perchlorate. Significant dose response (p<0.01) increases in uptake were observed following incubation with maximum uptakes (60% increase) at 100,000mIU/ml hCG; (45% increase) 200 IU/ml Oxytocin; (32% increase) 200µIU/ml Prolactin. Progesterone (0-2000ng/ml) and 17β-estradiol (0-900pg/ml) produced no significant difference in uptake of iodide.
These studies indicate the role of pregnancy associated hormones in promoting placental iodide uptake and are consistent with our previous finding that the placenta is an iodine storage organ with a potential role in compensating fetal iodine supply when maternal dietary iodine intake is deficient.