Swimming motions evoke Ca2+ events in vascular endothelial cells of larval zebrafish via mechanical activation of Piezo1

Abstract

Calcium signaling in blood vessels regulates their growth1,2, immune response3, and vascular tone4. Vascular endothelial cells are known to be mechanosensitive5-7, and it has been assumed that this mechanosensation mediates calcium responses to pulsatile blood flow8-10. Here we show that in larval zebrafish, the dominant trigger for vascular endothelial Ca2+ events comes from body motion, not heartbeat-driven blood flow. Through a series of pharmacological and mechanical perturbations, we showed that body motion is necessary and sufficient to induce endothelial Ca2+ events, while neither neural activity nor blood circulation is either necessary or sufficient. Knockout and temporally restricted knockdown of piezo1 eliminated the motion-induced Ca2+ events. Our results demonstrate that swimming-induced tissue motion is an important driver of endothelial Ca2+ dynamics in larval zebrafish. HighlightsO_LISwimming motions in larval zebrafish evoke large, rapid, and pervasive Ca2+ transients in vascular endothelial cells. C_LIO_LIThese Ca2+ transients do not require neural firing, muscular electrical activity, endocrine factors, or heart-driven blood flow. C_LIO_LIMechanical forces are necessary and sufficient for endothelial Ca2+ transients. C_LIO_LIEndothelial Ca2+ transients require the mechanosensitive ion channel Piezo1. C_LI