Defective rapid cell shape and transendothelial migration by calpain-1 null neutrophils.

It has been proposed that Ca²⁺ activation of calpain-1 is an important trigger for rapid cell spreading by neutrophils. In this paper, we have investigated this by assessing the ex vivo functioning of neutrophils from calpain-1 null mice, Calpain-1 null neutrophils failed to migrate through TNF-activated endothelial monolayers. The failure to transmigrate through endothelial monolayers was therefore unlikely to be due to a failure of chemotaxis as chemotaxis by adherent calpain-1 null neutrophils towards fMLP was unpaired. In contrast, the capacity of calpian-1 neutrophils to spontaneously spread was limited to smaller diameters than for wild type cells. Photolytic uncaging of IP₃ with Individual wild type neutrophils resulted in a large Ca²⁺ signal and rapid cell spreading. In contrast, calpain-1 neutrophils failed to spread in response to the IP₃-induced Ca²⁺ signal. This work has therefore demonstrated that the presence of calpain-1 was required for effective rapid cell spreading by neutrophils.

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