Authors Moon, Ko, and Jung contributed equally to this work.
H: HEALTH, NUTRITION, AND FOOD
Coenzyme Q10 Regulates Osteoclast and Osteoblast Differentiation
Version of Record online: 12 APR 2013
© 2013 Institute of Food Technologists®
Journal of Food Science
Volume 78, Issue 5, pages H785–H791, May 2013
How to Cite
Moon, H.-J., Ko, W.-K., Jung, M.-S., Kim, J. H., Lee, W.-J., Park, K.-S., Heo, J.-K., Bang, J. B. and Kwon, I. K. (2013), Coenzyme Q10 Regulates Osteoclast and Osteoblast Differentiation. Journal of Food Science, 78: H785–H791. doi: 10.1111/1750-3841.12116
- Issue online: 6 MAY 2013
- Version of Record online: 12 APR 2013
- Manuscript Accepted: 17 FEB 2013
- Manuscript Received: 16 OCT 2012
- Basic Research Program of the Korea Science & Engineering Foundation. Grant Number: 2012-0006171
- Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, Forestry and Fisheries. Grant Number: 312062-5
- National Research Foundation of Korea funded by the ministry of Education. Grant Number: 2012-0000443
- coenzyme Q10;
- matrix mineralization;
Coenzyme Q10 (CoQ10), a powerful antioxidant, is a key component in mitochondrial bioenergy transfer, generating energy in the form of ATP. Many studies suggest that antioxidants act as inhibitors of osteoclastogenesis and we also have previously demonstrated the inhibitory effect of CoQ10 on osteoclast differentiation. Despite the significance of this effect, the molecular mechanism when CoQ10 is present at high concentrations in bone remodeling still remains to be elucidated. In this study, we investigated the inhibitory effect of CoQ10 on osteoclastogenesis and its impact on osteoblastogenesis at concentrations ranging from 10 to 100 μM. We found that nontoxic CoQ10 markedly attenuated the formation of receptor activator of nuclear factor κB ligand (RANKL)-induced tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells in both bone-marrow-derived monocytes (BMMs) and RAW 264.7 cells. Osteoclastogenesis with CoQ10 was significantly suppressed the gene expression of NFATc1, TRAP, and osteoclast-associated immunoglobulin-like receptor, which are genetic markers of osteoclast differentiation and scavenged intracellular reactive oxygen species, an osteoclast precursor, in a dose-dependent manner. Furthermore, CoQ10 strongly suppressed H2O2-induced IκBα, p38 signaling pathways for osteoclastogenesis. In bone formation study, CoQ10 acted to enhance the induction of osteoblastogenic biomarkers including alkaline phosphatase, type 1 collagen, bone sialoprotein, osteoblast-specific transcription factor Osterix, and Runt-related transcription factor 2 and, also promoted matrix mineralization by enhancing bone nodule formation in a dose-dependent manner. Together, CoQ10 acts as an inhibitor of RANKL-induced osteoclast differentiation and an enhancer of bone-forming osteoblast differentiation. These findings highlight the potential therapeutic applications of CoQ10 for the treatment of bone disease.
CoQ10 suppresses osteoclast differentiation through H2O2-induced IκBα, p38 signaling pathways and enhances bone regeneration at all processes of differentiation through Runx2, Osterix activity. CoQ10 may potentially be useful for the treatment of osteoporosis and other bone diseases associated with excessive bone resorption.