Nature communications · 2026
Placental TRPV2 supports trophoblast function and normal fetal development.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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De Clercq Katrien, Pérez-García Vicente, Panda Amitesh, Gevaert Seppe, Witvrouwen Jill, Van Mechelen Pilar, Lopez-Tello Jorge, Maksym Katarzyna, David Anna L, Van Den Broeck Evy, Luyten Katrien, Segal Andrei, Poovathingal Suresh, Wojno Marta, Katanosaka Yuki, Vennekens Rudi, Pasque Vincent, Sferruzzi-Perri Amanda N, Voets Thomas, Vriens Joris
Аннотация
While placental functioning arbitrates fetal outcome, the molecular players that underpin normal placental development remain poorly understood. Here, we provide evidence that the Transient Receptor Potential Vanilloid 2 (TRPV2) channel plays an important role in normal placental development, determining fetal size and survival. Its absence severely affects placental morphology, causing fetal growth restriction and embryonic lethality, which was found to be allocated to a non-redundant role in the trophoblast, but not in the embryo. CRISPR/Cas9-mediated Trpv2 deletion in mouse trophoblast stem cells demonstrated that Trpv2 contributes to the differentiation towards Syncytiotrophoblast layer II (SynTII) cells, which was confirmed by the growth restriction phenotype in SynTII-specific Trpv2 knockout animals. Finally, TRPV2 was functionally expressed in human trophoblast cells and enriched in trophoblast populations undergoing syncytial differentiation. Together, our findings identify an important role for TRPV2 during placental development and consequently fetal outcomes.