Ca2+ and calpain control membrane expansion during rapid cell spreading of neutrophils

Dewitt, Sharon ORCID: https://orcid.org/0000-0001-8169-8241, Francis, Robert J. and Hallett, Maurice Bartlett ORCID: https://orcid.org/0000-0001-8197-834X 2013. Ca2+ and calpain control membrane expansion during rapid cell spreading of neutrophils. Journal of Cell Science 126 (20) , pp. 4627-4635. 10.1242/jcs.124917

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Abstract

Following adherence of neutrophils to the endothelium, neutrophils undergo a major morphological change which is a necessary prelude to their extravasation. We show here that this shape change is triggered by an elevation of cytosolic IP3, to provoke physiological Ca2+ influx through a store-operated mechanism. This transition from a spherical to “flattened” neutrophil morphology is rapid (about 100 s) and is accompanied by an apparent rapid expansion of the area of the plasma membrane. However, no new membrane is added into the plasma membrane. Pharmacological inhibition of calpain-activation, which is triggered by Ca2+ influx during neutrophil spreading, prevents normal cell flattening. In calpain-suppressed cells, an aberrant form of cell spreading can occur where an uncoordinated and localised expansion of the plasma membrane is evident. These data show that rapid neutrophil spreading is triggered by Ca2+ influx which causes activation of calpain, and release of furled plasma membrane to allow its apparent “expansion”.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Dentistry Medicine
Subjects:	R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords:	Ca2+ signalling; Cell spreading; Neutrophils; Phagocytosis; Inositol (1,4,5)-trisphosphate; IP3
Publisher:	The Company of Biologists
ISSN:	0021-9533
Last Modified:	25 Oct 2022 08:02
URI:	https://orca.cardiff.ac.uk/id/eprint/51169

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