Piezo1 expression in neutrophils regulates shear-induced NETosis

Sara Baratchi (), Habiba Danish, Chanly Chheang, Ying Zhou, Angela Huang, Austin Lai, Manijeh Khanmohammadi, Kylie M. Quinn, Khashayar Khoshmanesh and Karlheinz Peter
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Sara Baratchi: Baker Heart and Diabetes Institute
Habiba Danish: RMIT University
Chanly Chheang: Baker Heart and Diabetes Institute
Ying Zhou: Baker Heart and Diabetes Institute
Angela Huang: Baker Heart and Diabetes Institute
Austin Lai: Baker Heart and Diabetes Institute
Manijeh Khanmohammadi: RMIT University
Kylie M. Quinn: RMIT University
Khashayar Khoshmanesh: RMIT University
Karlheinz Peter: Baker Heart and Diabetes Institute

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract Neutrophil infiltration and subsequent extracellular trap formation (NETosis) is a contributing factor in sterile inflammation. Furthermore, neutrophil extracellular traps (NETs) are prothrombotic, as they provide a scaffold for platelets and red blood cells to attach to. In circulation, neutrophils are constantly exposed to hemodynamic forces such as shear stress, which in turn regulates many of their biological functions such as crawling and NETosis. However, the mechanisms that mediate mechanotransduction in neutrophils are not fully understood. In this study, we demonstrate that shear stress induces NETosis, dependent on the shear stress level, and increases the sensitivity of neutrophils to NETosis-inducing agents such as adenosine triphosphate and lipopolysaccharides. Furthermore, shear stress increases intracellular calcium levels in neutrophils and this process is mediated by the mechanosensitive ion channel Piezo1. Activation of Piezo1 in response to shear stress mediates calpain activity and cytoskeleton remodeling, which consequently induces NETosis. Thus, activation of Piezo1 in response to shear stress leads to a stepwise sequence of cellular events that mediates NETosis and thereby places neutrophils at the centre of localized inflammation and prothrombotic effects.

Date: 2024
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DOI: 10.1038/s41467-024-51211-1

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