Journal
JOURNAL OF BIOCHEMISTRY
Volume 129, Issue 6, Pages 963-969Publisher
JAPANESE BIOCHEMICAL SOC
DOI: 10.1093/oxfordjournals.jbchem.a002944
Keywords
Apaf1; apoptosis; electron microscopy; mitochondria; necrosis
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Apaf1 is a critical molecule in the mitochondria-dependent apoptotic pathway. Here we show that Apaf1-deficient embryonic fibroblasts died at a later phase of apoptotic induction, although these cells were resistant to various apoptotic stimulants at an early phase. Neither caspase 3 activation nor nuclear condensation was observed during this cell death of Apaf1-deficient cells, Electron microscopic examination revealed that death in response to apoptotic stimulation resembled necrosis ill that nuclei were round and swollen with low electron density. Necrosis-like cell death was also observed in wildtype cells treated with z-VAD-fmk. Mitochondria were not only morphologically abnormal but functionally affected, since mitochondrial transmembrane potential (Delta Psim) was lost even in cells with intact plasma membrane integrity, These mitochondrial alterations were also observed in the wild-type cells dying of apoptosis, Combined, these data suggest that cells without caspase activation, such as Apaf1-deficient cells or cells treated with caspase inhibitors, die of necrosis-like cell death with mitochondrial damage in response to apoptotic stimulation.
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