Endocrine Abstracts

Introduction: Placenta has many essential roles to maintain pregnancy and homeostasis. Calcium transport and its regulation are also important for vital roles of placenta. In general, calcium transport is regulated by active transcellular and passive paracellular pathways. Transient receptor potential cation channel subfamily V member 5/6 (TRPV5/6), calbindin-D9k (CaBP-9k), calbindin-D28k (CaBP-28k), and Na+/Ca2+ exchanger (NCX1) are involved in the transcellular pathway. Paracellular pathway is determined by expression of tight junction genes such as occludin, claudin, and ZO-1.

Methods: We examined whether the transcellular and paracellular calcium transport genes are differentially modulated in the placenta of CaBP-9k and/or CaBP-28k knockout (KO) mice on gestational day 19 (GD 19). The expressions of transcellular calcium transport and paracellular tight junction genes in the placenta were examined using real-time PCR and western blot analysis.

Results: The mRNA and protein expressions of calcium transport genes appeared to be increased in a compensatory manner. The expression levels of NCX1 and TPRV6 were increased at both mRNA and protein in KO compared to wild-type (WT) mice. CaBP-9k mRNA and protein were significantly induced in CaBP-28k KO mice, whereas these levels of CaBP-28k were reduced in the placenta of CaBP-9k mice compared to WT mice. Each tight junction gene was shown to be similarly expressed after ablation of CaBP-9k or CaBP-28k. Occludin and claudin levels were increased in single, CaBP-9k and CaBP-28k, KO mice, but not in double KO mice.

Conclusions: The disability of calcium buffering due to CaBP-9k and/or CaBP-28k KO, may lead to accelerate transcellular pathway of calcium, and also to decrease paracellular permeability through the tight junction to maintain calcium homeostasis in placenta of mice.

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.