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Am J Physiol Lung Cell Mol Physiol 275: L771-L779, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 4, L771-L779, October 1998

Tobacco smoke induces both apoptosis and necrosis in mammalian cells: differential effects of HSP70

Muriel Vayssier1, Nathalie Banzet1, Dominique François1, Kerstin Bellmann2, and Barbara S. Polla1,3

1 Laboratoire de Physiologie Respiratoire, Unité de Formation et de Recherche Cochin Port-Royal, 75014 Paris, France; 2 Diabetes Research Institute, Heinrich-Heine University, 40225 Düsseldorf, Germany; and 3 Environment and Health Program, Faculty of Medicine, University Hospital, 1211 Geneva 14, Switzerland

Tobacco smoke (TS) has been implicated as a major risk factor in human pulmonary diseases including cancer. In this study, we used TS as a model of oxidative stress. TS-mediated oxidative stress has been shown to induce protein oxidation, DNA damage, and cell death. Here we investigated, in human and rodent cell lines, whether TS induces cell death by apoptosis or by necrosis. As described for classic oxidants, TS induced apoptosis at low concentrations and necrosis at higher concentrations. We have previously described the induction of heat shock (HS) protein (HSP) (in particular, HSP70) in human monocytes exposed to TS. HSP70 is implicated in the regulation of cell injury and cell death and, in particular, modulates apoptosis, as does the antiapoptotic oncoprotein Bcl-2. At both apoptotic and necrotic concentrations, TS induced a dose-dependent HSP70 expression, whereas Bcl-2 was induced only at necrotic concentrations. TS- or HS-induced HSP had no protective effects either on apoptosis or on necrosis, but HSP70 overexpression prevented TS-induced necrosis and consequently led to increased apoptosis. These results might reconcile the apparently contradictory data previously reported on the effects of HSP on apoptosis.

heat shock protein 70; Bcl-2


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