Swimming motions evoke Ca 2+ events in vascular endothelial cells of larval zebrafish via mechanical activation of Piezo1

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Abstract

Calcium signaling in blood vessels regulates their growth 1,2 , immune response 3 , and vascular tone 4 . Vascular endothelial cells are known to be mechanosensitive 5–7 , and it has been assumed that this mechanosensation mediates calcium responses to pulsatile blood flow 8–10 . Here we show that in larval zebrafish, the dominant trigger for vascular endothelial Ca 2+ 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 Ca 2+ events, while neither neural activity nor blood circulation is either necessary or sufficient. Knockout and temporally restricted knockdown of piezo1 eliminated the motion-induced Ca 2+ events. Our results demonstrate that swimming-induced tissue motion is an important driver of endothelial Ca 2+ dynamics in larval zebrafish.

Highlights

  • Swimming motions in larval zebrafish evoke large, rapid, and pervasive Ca 2+ transients in vascular endothelial cells.

  • These Ca 2+ transients do not require neural firing, muscular electrical activity, endocrine factors, or heart-driven blood flow.

  • Mechanical forces are necessary and sufficient for endothelial Ca 2+ transients.

  • Endothelial Ca 2+ transients require the mechanosensitive ion channel Piezo1.

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