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Peroxiredoxin III, a mitochondrion-specific peroxidase, regulates apoptotic signaling by mitochondria

Title
Peroxiredoxin III, a mitochondrion-specific peroxidase, regulates apoptotic signaling by mitochondria
Authors
Chang T.-S.Cho C.-S.Park S.Yu S.Sang W.K.Sue G.R.
Ewha Authors
이서구강상원창동신
SCOPUS Author ID
이서구scopusscopus; 강상원scopus; 창동신scopus
Issue Date
2004
Journal Title
Journal of Biological Chemistry
ISSN
0021-9258JCR Link
Citation
Journal of Biological Chemistry vol. 279, no. 40, pp. 41975 - 41984
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Various proapoptotic stimuli increase the production of superoxide and H 2O 2 by mitochondria. Whereas superoxide impairs mitochondrial function and is removed by Mn 2+-dependent superoxide dismutase, the role and metabolism of mitochondrial H 2O 2 during apoptosis have remained unclear. The effects on apoptotic signaling of depletion of peroxiredoxin (Prx) III, a mitochondrion-specific H 2O 2-scavenging enzyme, have now been investigated by RNA interference in HeLa cells. Depletion of Prx III resulted in increased intracellular levels of H 2O 2 and sensitized cells to induction of apoptosis by staurosporine or TNF-α. The rates of mitochondrial membrane potential collapse, cytochrome c release, and caspase activation were increased in Prx III-depleted cells, and these effects were reversed by ectopic expression of Prx III or mitochondrion-targeted catalase. Depletion of Prx III also exacerbated damage to mitochondrial macromolecules induced by the proapoptotic stimuli. Our results suggest that Prx III is a critical regulator of the abundance of mitochondrial H 2O 2, which itself promotes apoptosis in cooperation with other mediators of apoptotic signaling.
DOI
10.1074/jbc.M407707200
Appears in Collections:
일반대학원 > 생명·약학부 > Journal papers
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