Keywords

The placental circulation is crucial for the development of mammalian embryos [1]. The labyrinth layer in the placenta is created by extensive villous branching of the trophoblast and vascularization arising from the embryonic mesoderm. In the labyrinth, materials are exchanged between the maternal and embryonic circulation. Recently, we have found that inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) may be required for the placental vascularization.

IP3Rs are intracellular Ca2+ release channels that have three subtypes in mammals (IP3R1, IP3R2 and IP3R3) [2]. We previously showed that IP3R1 and IP3R2 played an essential role in heart development from the analysis of mouse embryo double knockout for IP3R1 and IP3R2 [3]. A previous report on the requirement for phospholipase (PLC) δ1 and δ3 [4] that produce IP3 for placentation led us to investigate the placental defects by deletion of any subtypes of IP3Rs. Our preliminary result revealed that embryonic vasculature in the labyrinth was impaired in the placenta double knockout for IP3R1 and IP3R3 at E9.25 (Fig. 32.1). The detailed phenotype and the underlying mechanism how the intracellular Ca2+ signaling via IP3Rs may be implicated in the development of extraembryonic vasculature are under investigation.

Fig. 32.1
figure 1

Cross sections of E9.25 placentas from the IP3R1+/−3−/− (a and b) and IP3R1−/−3−/− (c and d) mice. (b) and (d) show higher-power fields of the rectangular areas of the labyrinth in (a) and (c), respectively. Embryonic vessels (arrowheads) fail to elongate to the maternal sinuses in the placenta of IP3R1−/−3−/− compared to that of IP3R1+/−3−/− (wild type). al allantois, de decidua, gi trophoblast giant cells, la labyrinth layer, sp spongiotrophoblast layer. Scale bars, 0.5 mm in (a) and (c) and 0.2 mm in (b) and (d)

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This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan (to K.U. and H.Y.).