Binet, François; Chiasson, Sonia et Girard, Denis 
ORCID: https://orcid.org/0000-0002-3342-5027
(2010).
Evidence that endoplasmic reticulum (ER) stress and caspase-4 activation occur in human neutrophils
Biochemical and Biophysical Research Communications
, vol. 391
, nº 1.
pp. 18-23.
DOI: 10.1016/j.bbrc.2009.10.141.
Résumé
Apoptosis can result from activation of three major pathways: the extrinsic, the intrinsic, and the most recently identified endoplasmic reticulum (ER) stress-mediated pathway. While the two former pathways are known to be operational in human polymorphonuclear neutrophils (PMNs), the existence of the ER stress-mediated pathway, generally involving caspase-4, has never been reported in these cells. Recently, we have documented that arsenic trioxide (ATO) induced apoptosis in human PMNs by a mechanism that needs to be further investigated. In this study, using immunofluorescence and electron microscopy, we present evidence of ER alterations in PMNs activated by the ER stress inducer arsenic trioxide (ATO). Several key players of the unfolded protein response, including GRP78, GADD153, ATF6, XBP1 and eIF2α are expressed and activated in PMNs treated with ATO or other ER stress inducers. Although caspase-4 is expressed and activated in neutrophils, treatment with a caspase-4 inhibitor did not attenuate the pro-apoptotic effect of ATO at a concentration that reverses caspase-4 processing and activation. Our results demonstrate for the first time that the ER stress-mediated apoptotic pathway operates in human neutrophils.
| Type de document: | Article |
|---|---|
| Mots-clés libres: | Apoptosis; Endoplasmic reticulum; Caspase-4; Neutrophils |
| Centre: | Centre INRS-Institut Armand Frappier |
| Date de dépôt: | 29 juin 2024 21:34 |
| Dernière modification: | 29 juin 2024 21:34 |
| URI: | https://espace.inrs.ca/id/eprint/14418 |
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