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

Ishak, Reezal and Hallett, Maurice B. 2018. Defective rapid cell shape and transendothelial migration by calpain-1 null neutrophils. Biochemical and Biophysical Research Communications 506 (4) , pp. 1065-1070. 10.1016/j.bbrc.2018.10.174

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Abstract

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.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: Elsevier
ISSN: 0006-291X
Date of Acceptance: 28 October 2018
Last Modified: 04 Feb 2019 11:01
URI: http://orca.cf.ac.uk/id/eprint/119093

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