This process is crucial for many biological structures, such as blood vessels, to develop correctly, and is also a key part of our senses of touch and hearing. These mechanical forces are then transformed into electrical or chemical signals by cells. Within our bodies, cells and tissues are constantly being pushed and pulled by their surrounding environment. Therefore, mechanically activated Piezo1 plays an essential role in RBC volume homeostasis. Finally, we show that Yoda1, a chemical activator of Piezo1, causes calcium influx and subsequent dehydration of RBCs via downstream activation of the KCa3.1 Gardos channel, directly implicating Piezo1 signaling in RBC volume control. Furthermore, RBCs from blood-cell-specific Piezo1 conditional knockout mice are overhydrated and exhibit increased fragility both in vitro and in vivo. In this study, we show that RBCs exhibit robust calcium entry in response to mechanical stretch and that this entry is dependent on Piezo1 expression. However, the mechanisms by which these mutations result in RBC dehydration are unknown. ![]() ![]() ![]() Recent work has shown that gain-of-function mutations in mechanically activated Piezo1 cation channels are associated with the dehydrating RBC disease xerocytosis, implicating a role of mechanotransduction in RBC volume regulation. Red blood cells (RBCs) experience significant mechanical forces while recirculating, but the consequences of these forces are not fully understood.
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