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Ca2+ influx shutdown in neutrophils induced by Fas (CD95) cross-linking

Ayub, Khurram, Laffaffian, Iraq, Dewitt, Sharon and Hallett, Maurice Bartlett 2004. Ca2+ influx shutdown in neutrophils induced by Fas (CD95) cross-linking. Immunology 112 (3) , pp. 454-460. 10.1111/j.1365-2567.2004.01899.x

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Abstract

In neutrophils, as in most other cell types, Ca2+ signalling is important for a number of cellular activities. Although inositol(1,4,5)trisphosphate-mediated release of Ca2+ from intracellular stores is a necessary prelude, it is the Ca2+ influx that is responsible for many of the neutrophil responses. We report here that although elevations of cytosolic Ca2+ do not accompany Fas-mediated apoptosis in neutrophils, the Ca2+ influx component of the response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) becomes selectively inactived as the neutrophils progress towards accelerated apoptosis induced by Fas (CD95) cross-linking. After 4 hr incubation at 37°, untreated neutrophils display an exaggerated Ca2+ influx phase in response to FMLP. This was absent in neutrophils that had been Fas-activated at the same time. No Ca2+ influx component was demonstrable by the removal of extracellular Ca2+ or by Ca2+ channel blockade with Ni2+ and no Mn2+ influx was detectable. The defect could not be attributed to a decrease in receptor sensitivity, receptor coupling or receptor number because the release of stored Ca2+ remained constant during incubation and was unaffected by Fas activation. Ca2+ influx became uncoupled from store release before detectable gross morphological changes or phosphatidyl serine externalization and was also insensitive to caspase 3 and 8 inhibitors. These results suggest a mechanism other than caspase-mediated proteolytic damage to components important for Ca2+ influx.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
R Medicine > RZ Other systems of medicine
Publisher: Wiley Blackwell
ISSN: 0019-2805
Last Modified: 25 Jan 2018 10:41
URI: http://orca-mwe.cf.ac.uk/id/eprint/72725

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