Ferroportin gene and protein expression in human IUGR placentas

Iron (Fe) deficiency in pregnancy is associated with low birth weight and premature delivery. We demonstrated a significant decrease of the Fe cell-importer Transferrin Receptor (TfR1) in human Intrauterine Growth Restricted (IUGR) vs normal (N) placentas. Ferroportin (FPN), located in the trophoblast cell (TC) basal membrane, exports Fe towards the fetal circulation. We hypothesized that TfR1 downregulation in IUGR placentas could be due to Fe intracellular accumulation, and we measured FPN expression in human IUGR vs N placentas. Placentas were sampled at the time of elective cesarean section; villi were selected, washed and immediately frozen for following analysis. IUGR was defined by a reduction of more than 40 centiles in the growth of the abdominal circumference measured by ultrasound in utero and birth weight <10th percentile. Three severity groups were identified depending on the umbilical artery pulsatility index and fetal heart rate. FPN mRNA was quantified in 41 IUGR and 50 N placentas by Real Time PCR. Among them, we measured FPN protein expression in 14 IUGR and 26 N placentas, setting up a specific Enzyme-Linked ImmunoSorbent Assay (Elisa) protocol. Both FPN mRNA and protein expression were not statistically different in IUGR vs N placentas, independently from the degree of severity. Our results show no differences in IUGR and N FPN mRNA and protein placental levels. This suggests that Fe is not accumulated in IUGR TC, and the Fe reaching IUGR fetuses could be decreased compared to normal pregnancies, as a consequence of TfR1 downregulation in the microvillous membranes. Since FPN is known to be post-transcriptionally finely regulated, we aim at enlarging our Elisa analysis case study in order to confirm our data, and then measuring Fe levels in the cord blood to verify our hypothesis.