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Human & Experimental Toxicology, Vol. 22, No. 12, 629-637 (2003)
DOI: 10.1191/0960327103ht403oa

Mechanisms involved in methylmercuric chloride (MeHgCl)-induced suppression of human neutrophil apoptosis

éliane Moisan

NRS-Institut Armand-Frappier, Université du Québec, 245 boulevard Hymus, Pointe-Claire (PQ), Canada

édouard Kouassi

Maisonneuve-Rosemont Hospital, Research Center, Montreal, PQ, Canada

Denis Girard

INRS-Institut Armand-Frappier, Université du Québec, 245 boulevard Hymus, Pointe-Claire (PQ), Canada, INRS-Institut Armand-Frappier, 245 boul. Hymus, Pointe-Claire (PQ), Canada, H9R 1G6, denis.girard{at}inrs-iaf.uquebec.ca

We have previously demonstrated that concentrations of 1-10 µM 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 M MeHgCl inducesde 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 novoprotein 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.

Key Words: apoptosis • cytoskeleton • inflammation • Mcl-1 • mercury • neutrophil


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 J. Leukoc. Biol.Home page
E. Moisan and D. Girard
Cell surface expression of intermediate filament proteins vimentin and lamin B1 in human neutrophil spontaneous apoptosis
J. Leukoc. Biol., March 1, 2006; 79(3): 489 - 498.
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