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Vol. 13, Issue 3, 978-988, March 2002
*Department of Immunology and Cell Biology, University of
Münster, Münster, Germany; Death ligands not only induce apoptosis but can also trigger
necrosis with distinct biochemical and morphological features. We
recently showed that in L929 cells CD95 ligation induces apoptosis, whereas TNF elicits necrosis. Treatment with anti-CD95 resulted in
typical apoptosis characterized by caspase activation and DNA fragmentation. These events were barely induced by TNF, although TNF
triggered cell death to a similar extent as CD95. Surprisingly, whereas
the caspase inhibitor zVAD prevented CD95-mediated apoptosis, it
potentiated TNF-induced necrosis. Cotreatment with TNF and zVAD was
characterized by ATP depletion and accelerated necrosis. To investigate
the mechanisms underlying TNF-induced cell death and its potentiation
by zVAD, we examined the role of poly(ADP-ribose)polymerase-1 (PARP-1).
TNF but not CD95 mediated PARP activation, whereas a PARP inhibitor
suppressed TNF-induced necrosis and the sensitizing effect of zVAD. In
addition, fibroblasts expressing a noncleavable PARP-1 mutant were more
sensitive to TNF than wild-type cells. Our results indicate that TNF
induces PARP activation leading to ATP depletion and subsequent
necrosis. In contrast, in CD95-mediated apoptosis caspases cause PARP-1
cleavage and thereby maintain ATP levels. Because ATP is required for
apoptosis, we suggest that PARP-1 cleavage functions as a molecular
switch between apoptotic and necrotic modes of death receptor-induced
cell death.
Department of
Experimental and Diagnostic Medicine, University of Ferrara, Ferrara,
Italy; and §International Agency for Research on Cancer
(IARC), Lyon, France
Corresponding author. E-mail address:
los{at}uni-muenster.de.
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