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Widespread mitochondrial depletion via mitophagy does not compromise necroptosis.

Abstract : Programmed necrosis (or necroptosis) is a form of cell death triggered by the activation of receptor interacting protein kinase-3 (RIPK3). Several reports have implicated mitochondria and mitochondrial reactive oxygen species (ROS) generation as effectors of RIPK3-dependent cell death. Here, we directly test this idea by employing a method for the specific removal of mitochondria via mitophagy. Mitochondria-deficient cells were resistant to the mitochondrial pathway of apoptosis, but efficiently died via tumor necrosis factor (TNF)-induced, RIPK3-dependent programmed necrosis or as a result of direct oligomerization of RIPK3. Although the ROS scavenger butylated hydroxyanisole (BHA) delayed TNF-induced necroptosis, it had no effect on necroptosis induced by RIPK3 oligomerization. Furthermore, although TNF-induced ROS production was dependent on mitochondria, the inhibition of TNF-induced necroptosis by BHA was observed in mitochondria-depleted cells. Our data indicate that mitochondrial ROS production accompanies, but does not cause, RIPK3-dependent necroptotic cell death.
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Submitted on : Thursday, October 20, 2016 - 10:50:41 AM
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Widespread mitochondrial deple...
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Stephen w.G. Tait, Andrew Oberst, Giovanni Quarato, Sandra Milasta, Martina Haller, et al.. Widespread mitochondrial depletion via mitophagy does not compromise necroptosis.. Cell Reports, Elsevier Inc, 2013, 5 (4), pp.438-41. ⟨10.1016/j.celrep.2013.10.034⟩. ⟨pasteur-01384556⟩



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