Yoshiro Suzuki, Soshi Otani, Shouichi Shibasaki, Keishi Otsu, Katsumi Nakajima
Maternal-fetal calcium (Ca2 +) transport through the placenta is crucial for the development of fetal organs including bones. Although we have reported that the transient receptor potential cation channel, subfamily V, member 6 (TRPV6) was responsible for the maternal-fetal Ca2+ transport, there has been no direct evidence for its channel activity in placental trophoblasts. By using human trophoblast stem cells, we observed biphasic higher intracellular Ca2+ levels compared with undifferentiated cells during the differentiation of syncytiotrophoblasts. Second Ca2+ peak, when the syncytiotrophoblasts might mature with transport function, was found to be a Ca2+ flux through TRPV6. Unexpectedly we observed the first peak, when trophoblasts fuse to form syncytiotrophoblast. We found that it was derived through TRPV4, and blocking TRPV4 suppressed trophoblast cell fusion. Our results might provide the first evidence for TRPV6 channel activities in syncytiotrophoblasts involved in the maternal-fetal Ca2+ transport.