期刊
CELL REPORTS
卷 5, 期 4, 页码 878-885出版社
CELL PRESS
DOI: 10.1016/j.celrep.2013.10.034
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资金
- Royal Society
- BBSRC [BB/K008374/1]
- NIH [AI44828, CA169291]
- American Lebanese Charity
- Syrian Associated Charity
- BBSRC [BB/K008374/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K008374/1] Funding Source: researchfish
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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