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

Single, Barbara; Leist, Marcel; Nicotera, Pierluigi

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

Dateien

Single_2-rfx4nief4v8a7.pdfGröße: 421.26 KBDownloads: 311

Datum

2001

Autor:innen

Single, Barbara

Leist, Marcel

Nicotera, Pierluigi

Open Access-Veröffentlichung

Open Access Green

Sammlungen

Biologie

Publikationstyp

Zeitschriftenartikel

Publikationsstatus

Published

Erschienen in

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.

Fachgebiet (DDC)

570 Biowissenschaften, Biologie

Zitieren

ISO 690

SINGLE, 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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