Endocrine Abstracts

Introduction: Preeclampsia is a pregnancy-specific disease characterized by de novo development of concurrent hypertension, proteinuria and oxidative stress in the placenta. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Last trimester of gestation, the calcium and mineral transport from mother to fetus are dramatically increased in response to the accelerated demand for bone mineralization in the fetus. Two channels of this subfamily, TRPM6 and TRPM7, are permeable for various divalent cations, including Ca²⁺, Mg²⁺ and Zn²⁺. Adequate phosphate homeostasis is of critical importance for a wide variety of functions including bone mineralization and energy metabolism. Signaling mechanisms mediating hormonal regulation of Mg²⁺ and inorganic phosphate channels are not well understood in the placenta during pregnancy.

Methods: The expression of cell membrane Mg²⁺ and inorganic phosphate channels was investigated when oxidative stress was induced in human placental cells BeWo, JEG3 and human placental primary cells (hPC). The mRNA and protein levels were examined by real-time PCR and western blot analysis.

Results: The transcriptional and translational levels of Mg²⁺ and inorganic phosphate channels were altered in hypoxic condition. The expression of Mg²⁺ channels was down-regulated by hypoxia. The transcripts of inorganic phosphate channels were increased in BeWo and JEG3 cells, while decreased in the hPC.

Conclusions: Mg²⁺ and inorganic phosphate channels were distinctly expressed after oxidative stress in human placental cells, suggesting that altered expression of Mg²⁺ and inorganic phosphate channels may be involved in placental hypoxic stress, a determinant factor causing preeclamptic abnormality in human placental cells.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.