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RIP3-Dependent Accumulation of Mitochondrial Superoxide Anions in TNF-α-Induced Necroptosis
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Type
Academic journal
Author
Jiyoung Lee (Ewha Womans University) Sunmi Lee (Ewha Womans University) Seongchun Min (Ewha Womans University) Kang Sang Won (Ewha Womans University)
Journal
The Korean Society For Molecular And Cellular Biology Molecules and Cells Molecules and Cells 제45권 제4호 KCI Accredited Journals
Published
2022.4
Pages
193 - 201 (9page)
DOI
10.14348/molcells.2021.0260

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RIP3-Dependent Accumulation of Mitochondrial Superoxide Anions in TNF-α-Induced Necroptosis
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Excessive production of reactive oxygen species (ROS) is a key phenomenon in tumor necrosis factor (TNF)-α-induced cell death. However, the role of ROS in necroptosis remains mostly elusive. In this study, we show that TNF-α induces the mitochondrial accumulation of superoxide anions, not H2O2, in cancer cells undergoing necroptosis. TNF-α-induced mitochondrial superoxide anions production is strictly RIP3 expression-dependent. Unexpectedly, TNF-α stimulates NADPH oxidase (NOX), not mitochondrial energy metabolism, to activate superoxide production in the RIP3-positive cancer cells. In parallel, mitochondrial superoxide-metabolizing enzymes, such as manganese-superoxide dismutase (SOD2) and peroxiredoxin III, are not involved in the superoxide accumulation. Mitochondrial-targeted superoxide scavengers and a NOX inhibitor eliminate the accumulated superoxide without affecting TNF-α-induced necroptosis. Therefore, our study provides the first evidence that mitochondrial superoxide accumulation is a consequence of necroptosis.
#NADPH oxidase #necroptosis #superoxide anion #tumor necrosis factor-α

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