Differential Effects of Bcl-2 on Cell Death Triggered under ATP-Depleting Conditions

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2001
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Experimental Cell Research. 2001, 262(1), pp. 8-16. ISSN 0014-4827. eISSN 1090-2422. Available under: doi: 10.1006/excr.2000.5059
Zusammenfassung

The intracellular ATP concentration decides on the onset of either apoptosis or necrosis in Jurkat cells exposed to death stimuli. Bcl-2 can block apoptotic demise, which occurs preferably under conditions of high cellular ATP levels. Here, we investigated the effects of Bcl-2 on the necrotic type of cell demise that prevails under conditions of energy loss. ATP levels were modulated by using mitochondrial inhibitors, such as rotenone or S-nitrosoglutathione, in medium either lacking glucose or supplemented with glucose to stimulate glycolytic ATP generation. Under conditions of ATP depletion, staurosporine (STS) induced >90% necrosis in vector control-transfected cells, whereas bcl-2-transfected cells were protected. Thus, the antiapoptotic protein Bcl-2 can reduce the overall amount of cell death in ATP-depleted cells regardless whether it occurs by apoptosis or necrosis. Cytochrome c release, normally preceding STS-induced necrosis, was also inhibited by Bcl-2. However, Bcl-2 did not prevent an initial STS-induced drop of the mitochondrial membrane potential (DeltaPsi(m)). Therefore, the mechanisms whereby Bcl-2 prevents cell death and favors retention of cytochrome c in the mitochondria require neither the maintenance of mitochondrial DeltaPsi nor the maintenance of normal ATP levels.

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ISO 690SINGLE, Barbara, Marcel LEIST, Pierluigi NICOTERA, 2001. Differential Effects of Bcl-2 on Cell Death Triggered under ATP-Depleting Conditions. In: Experimental Cell Research. 2001, 262(1), pp. 8-16. ISSN 0014-4827. eISSN 1090-2422. Available under: doi: 10.1006/excr.2000.5059
BibTex
@article{Single2001-01-01Diffe-40513,
  year={2001},
  doi={10.1006/excr.2000.5059},
  title={Differential Effects of Bcl-2 on Cell Death Triggered under ATP-Depleting Conditions},
  number={1},
  volume={262},
  issn={0014-4827},
  journal={Experimental Cell Research},
  pages={8--16},
  author={Single, Barbara and Leist, Marcel and Nicotera, Pierluigi}
}
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    <dcterms:abstract xml:lang="eng">The intracellular ATP concentration decides on the onset of either apoptosis or necrosis in Jurkat cells exposed to death stimuli. Bcl-2 can block apoptotic demise, which occurs preferably under conditions of high cellular ATP levels. Here, we investigated the effects of Bcl-2 on the necrotic type of cell demise that prevails under conditions of energy loss. ATP levels were modulated by using mitochondrial inhibitors, such as rotenone or S-nitrosoglutathione, in medium either lacking glucose or supplemented with glucose to stimulate glycolytic ATP generation. Under conditions of ATP depletion, staurosporine (STS) induced &gt;90% necrosis in vector control-transfected cells, whereas bcl-2-transfected cells were protected. Thus, the antiapoptotic protein Bcl-2 can reduce the overall amount of cell death in ATP-depleted cells regardless whether it occurs by apoptosis or necrosis. Cytochrome c release, normally preceding STS-induced necrosis, was also inhibited by Bcl-2. However, Bcl-2 did not prevent an initial STS-induced drop of the mitochondrial membrane potential (DeltaPsi(m)). Therefore, the mechanisms whereby Bcl-2 prevents cell death and favors retention of cytochrome c in the mitochondria require neither the maintenance of mitochondrial DeltaPsi nor the maintenance of normal ATP levels.</dcterms:abstract>
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