Calcium channel TRPV6 is involved in murine maternal-fetal calcium transport

Yoshiro Suzuki, Christopher S. Kovacs, Hitomi Takanaga, Ji-Bin Peng, Christopher Paul Landowski, Matthias Hediger (Corresponding Author)

Research output: Contribution to journalArticleScientificpeer-review

79 Citations (Scopus)

Abstract

Maternal-fetal calcium (Ca(2+)) transport is crucial for fetal Ca(2+) homeostasis and bone mineralization. In this study, the physiological significance of the transient receptor potential, vanilloid 6 (TRPV6) Ca(2+) channel in maternal-fetal Ca(2+) transport was investigated using Trpv6 knockout mice. The Ca(2+) concentration in fetal blood and amniotic fluid was significantly lower in Trpv6 knockout fetuses than in wildtypes. The transport activity of radioactive Ca(2+) ((45)Ca) from mother to fetuses was 40% lower in Trpv6 knockout fetuses than in wildtypes. The ash weight was also lower in Trpv6 knockout fetuses compared with wildtype fetuses. TRPV6 mRNA and protein were mainly localized in intraplacental yolk sac and the visceral layer of extraplacental yolk sac, which are thought to be the places for maternal-fetal Ca(2+) transport in mice. These expression sites were co-localized with calbindin D(9K) in the yolk sac. In wildtype mice, placental TRPV6 mRNA increased 14-fold during the last 4 days of gestation, which coincides with fetal bone mineralization. These results provide the first in vivo evidence that TRPV6 is involved in maternal-fetal Ca(2+) transport. We propose that TRPV6 functions as a Ca(2+) entry pathway, which is critical for fetal Ca(2+) homeostasis.
Original languageEnglish
Pages (from-to)1249-56
JournalJournal of Bone and Mineral Research
Volume23
Issue number8
DOIs
Publication statusPublished - Aug 2008
MoE publication typeNot Eligible

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