Title: Mitochondria are targets for peroxisome-derived oxidative stress in cultured mammalian cells
Authors: Wang, Bo
Van Veldhoven, Paul P
Brees, Chantal
Rubio, N
Nordgren, Marcus
Ivashchenko en Apanasets, Oksana
Kunze, Markus
Baes, Myriam
Agostinis, Patrizia
Fransen, Marc # ×
Issue Date: Dec-2013
Publisher: Pergamon
Series Title: Free Radical Biology & Medicine vol:65 pages:882-894
Abstract: Many cellular processes are driven by spatially and temporally regulated redox-dependent signaling events. Although mounting evidence indicates that organelles such as the endoplasmic reticulum and mitochondria can function as signaling platforms for oxidative stress-regulated pathways, little is known about the role of peroxisomes in these processes. In this study, we employ targeted variants of the genetically-encoded photosensitizer KillerRed to gain a better insight into the interplay between peroxisomes and cellular oxidative stress. We show that the phototoxic effects of peroxisomal KillerRed induce mitochondria-mediated cell death, and that this process can be counteracted by targeted overexpression of a select set of antioxidant enzymes, including peroxisomal glutathione-S-transferase kappa 1, superoxide dismutase 1, and mitochondrial catalase. We also present evidence that peroxisomal disease cell lines deficient in plasmalogen biosynthesis or peroxisome assembly are more sensitive to KillerRed-induced oxidative stress than control cells. Collectively, these findings confirm and extend previous observations suggesting that disturbances in peroxisomal redox control and metabolism can sensitize cells for oxidative stress. In addition, they lend strong support to the ideas that peroxisomes and mitochondria share a redox-sensitive relationship, and that the redox communication between these organelles is not only mediated by diffusion of reactive oxygen species from one compartment to the other. Finally, these findings indicate that mitochondria may act as dynamic receivers, integrators, and transmitters of peroxisome-derived mediators of oxidative stress, and this may have profound implications for our views on cellular aging and age-related diseases.
ISSN: 0891-5849
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Lipid Biochemistry and Protein Interactions
Cell Metabolism
Laboratory of Cell Death Research & Therapy
× corresponding author
# (joint) last author

Files in This Item:
File Description Status SizeFormat
Wang et al_2013.pdfOA article Published 1679KbAdobe PDFView/Open


All items in Lirias are protected by copyright, with all rights reserved.

© Web of science