Placental TRPV2 supports trophoblast function and normal fetal development

Using a conditional knockout mouse model, we demonstrate that loss of Trpv2 leads to placental abnormalities characterized by impaired labyrinth organization and reduced vascularization. In situ hybridization reveal that Trpv2 is expressed in specific trophoblast subpopulations, including syncytiotrophoblast lineage cells.

To assess transcriptional consequences of Trpv2 loss at the tissue level, bulk RNA sequencing was performed on isolated placental labyrinth tissue from control and knockout embryos at mid- and late gestation stages. To complement the in vivo analysis, we generated Trpv2 knockout mouse trophoblast stem cells (mTSCs) using CRISPR/Cas9 and performed bulk RNA sequencing under stem and differentiation conditions. These experiments were designed to identify cell-autonomous transcriptional changes and to assess the role of TRPV2 in regulating trophoblast differentiation programs.