In vitro examination of Piezo1-TRPV4 dynamics: implications for placental endothelial function in normal and preeclamptic pregnancies
Hanna Allerkamp, Alexander I. Bondarenko, Ines Tawfik, Nilüfer Kamali-Simsek, Monika Horvat Merčnik, Corina T. Madreiter‐Sokolowski, Christian Wadsack
Abstract
This study shows Piezo-type mechanosensitive ion channel component 1 (Piezo1) and transient receptor potential cation channel subfamily V member 4 (TRPV4) coexpression and functionality within primary human fetoplacental endothelial cells (fpECs), mediating nitric oxide (NO) production and barrier integrity. In early-onset preeclampsia (EPE), fpEC channel functionality and coregulation are impaired, affecting Ca 2+ signaling and endothelial barrier function. Combined channel activation significantly reduces endothelial barrier integrity and increases NO production in EPE. Changes in arachidonic acid metabolism are suggested as a key underlying factor mediating impaired channel functionality in EPE fpECs.