Journal
SKELETAL BIOLOGY AND MEDICINE
Volume 1192, Issue -, Pages 245-252Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2009.05377.x
Keywords
mitochondrial ROS production; MitoQ; respiratory stress signaling; osteoclast differentiation; RAW 264.7 macrophages; TRAP-positive cells
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Funding
- National Institutes of Health (NIH) [CA-22762]
- Merck/NIH at the University of Pennsylvania, School of Veterinary Medicine [RR 07065]
- NATIONAL CANCER INSTITUTE [R01CA022762, R37CA022762] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [T35RR007065] Funding Source: NIH RePORTER
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Previously we showed that hypoxia-induced mitochondrial respiratory stress in RAW 264.7 macrophages and other cells caused activation of retrograde signaling (also known as mitochondrial respiratory stress signaling) and the appearance of tartrate-resistant acid phosphatase (TRAP)-positive cells. In the present study, we used N-acetyl cysteine and ascorbate (general antioxidants) and MitoQ, a mitochondria-specific antioxidant, to investigate the role of intracellular reactive oxygen species (ROS) in osteoclast differentiation. Our results show that hypoxia-mediated mitochondrial dysfunction, as tested by disruption of mitochondrial transmembrane potential, was suppressed by MitoQ as well as by the other antioxidants. These agents also suppressed the activation of mitochondrial retrograde signaling. Interestingly, in terms of molar concentrations, MitoQ was more than 1000-fold more effective than general antioxidants in suppressing the receptor activator of nuclear factor-B ligand-induced differentiation of RAW 264.7 cells into multinucleated and TRAP-positive osteoclasts. We propose that mitochondrial function and intramitochondrial ROS play important roles in osteoclastogenesis.
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