Preeclampsia is a pregnancy-specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal-to-fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca(2+) , Mg(2+) , and Zn(2+) . The regulation of magnesium/inorganic phosphorus ion-channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (TRPM6, TRPM7, PiT-1, and PiT-2) was down-regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor-although TRPM7 expression in the central placenta or PiT-2 expression in whole placenta was unchanged or up-regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT-1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT-2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down-regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor.
© 2014 Wiley Periodicals, Inc.