Moisan, Eliane; Kouassi, Edouard et Girard, Denis 
ORCID: https://orcid.org/0000-0002-3342-5027
(2003).
Mechanisms involved in methylmercuri chloride (MeHgCl)-induced suppression of human neutrophil apoptosis
Human and Experimental Toxicology
, vol. 22
, nº 12.
pp. 629-637.
DOI: 10.1191/0960327103ht403oa.
Résumé
We have previously demonstrated that concentrations of 1-10 microM of methylmercuric chloride (MeHgCl) that are cytotoxic to monocytes-macrophages can curiously inhibit neutrophil apoptosis by a yet unknown mechanism. In the present study, we demonstrate that, as with the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), a classical inhibitor of neutrophil apoptosis, treatment of cells with 5 microM MeHgCl induces de novo protein synthesis and prevents the loss of expression of the antiapoptotic Mcl-1 protein. The expression of the cytoskeletal proteins gelsolin, paxillin and vinculin was similar in MeHgCl- or GM-CSF-induced suppression of apoptosis. However, MeHgCl prevents the degradation of vimentin differently than GM-CSF. Apoptosis was further confirmed by flow cytometry (FITC annexin-V), and by monitoring CD16 cell surface expression. Curiously, unlike GM-CSF, MeHgCl did not prevent CD16 shedding. We conclude that, like GM-CSF, MeHgCl can delay neutrophil apoptosis by inducing de novo protein synthesis and by preventing the loss of the antiapoptotic Mcl-1 protein. However, unlike GM-CSF, MeHgCl induces an atypical degradation of vimentin without preventing CD16 shedding.
| Type de document: | Article |
|---|---|
| Mots-clés libres: | apoptosis; cytoskeleton; inflammation; Mcl-1; mercury; neutrophil |
| Centre: | Centre INRS-Institut Armand Frappier |
| Date de dépôt: | 25 déc. 2024 17:56 |
| Dernière modification: | 25 déc. 2024 17:56 |
| URI: | https://espace.inrs.ca/id/eprint/14979 |
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