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Calcium Channel TRPV6 Is Involved in Murine Maternal–Fetal Calcium Transport
Author(s) -
Suzuki Yoshiro,
Kovacs Christopher S,
Takanaga Hitomi,
Peng JiBin,
Landowski Christopher P,
Hediger Matthias A
Publication year - 2008
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.080314
Subject(s) - trpv6 , endocrinology , medicine , fetus , calcium , calcium metabolism , knockout mouse , homeostasis , calcium channel , biology , pregnancy , receptor , genetics
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 Trpv 6 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.