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, Haemin Kim Department of Cell and Developmental Biology, BK21 Program and DRISeoul National UniversitySeoulKorea Search for other works by this author on: Oxford Academic Yong Deok Lee Department of Cell and Developmental Biology, BK21 Program and DRISeoul National UniversitySeoulKorea Search for other works by this author on: Oxford Academic Hyung Joon Kim Department of Oral PhysiologySchool of DentistryPusan National UniversityYangsanKorea Search for other works by this author on: Oxford Academic Zang Hee Lee Department of Cell and Developmental Biology, BK21 Program and DRISeoul National UniversitySeoulKorea Search for other works by this author on: Oxford Academic Hong‐Hee Kim Department of Cell and Developmental Biology, BK21 Program and DRISeoul National UniversitySeoulKorea Address correspondence to: Hong‐Hee Kim, PhD, Department of Cell and Developmental Biology, BK21 Program and Dental Research Institute, Seoul National University, 101 Daehak‐ro, Jongro‐gu, Seoul 03080, Korea. E‐mail: hhbkim@snu.ac.kr Search for other works by this author on: Oxford Academic
Journal of Bone and Mineral Research, Volume 32, Issue 2, 1 February 2017, Pages 397–406, https://doi.org/10.1002/jbmr.2974
Published:
19 August 2016
Article history
Received:
13 April 2016
Revision received:
08 August 2016
Accepted:
16 August 2016
Published:
19 August 2016
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Haemin Kim, Yong Deok Lee, Hyung Joon Kim, Zang Hee Lee, Hong‐Hee Kim, SOD2 and Sirt3 Control Osteoclastogenesis by Regulating Mitochondrial ROS, Journal of Bone and Mineral Research, Volume 32, Issue 2, 1 February 2017, Pages 397–406, https://doi.org/10.1002/jbmr.2974
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ABSTRACT
Reactive oxygen species (ROS) are an indispensable element of cellular signal transduction in various cell types, including bone cells. In particular, osteoclasts (OCs), cells specialized for bone resorption, utilize ROS as second messengers during receptor activator of NF‐κB ligand (RANKL)‐induced differentiation and activation. In addition, because of the high energy demands of bone‐resorbing activity, OCs contain large amounts of mitochondria, the source of the majority of total ROS. In this study, we focused on the regulation of ROS generated from mitochondria during osteoclastogenesis. We observed that the level of mitochondrial superoxide dismutase 2 (SOD2), an enzyme responsible for reducing superoxide radicals in mitochondria, was increased by RANKL. siRNA‐mediated knockdown (KD) of SOD2 increased ROS levels and enhanced OC differentiation. Conversely, overexpression of SOD2 reduced osteoclastogenesis by decreasing ROS levels. Moreover, we found that NAD‐dependent deacetylase sirtuin 3 (Sirt3), an activator of SOD2 in mitochondria, was induced by RANKL. Sirt3‐targeted siRNA decreased SOD2 activity by reducing deacetylation of lysine 68 of SOD2, leading to increased osteoclastogenesis. Furthermore, in vivo KD of SOD2 or Sirt3 in ICR mouse calvariae decreased bone volume and increased OC surface, supporting the results of in vitro experiments. Taken together, our findings demonstrate for the first time to our knowledge that the regulation of mitochondrial ROS by SOD2 and Sirt3 plays an important role in fine‐tuning the OC differentiation program. © 2016 American Society for Bone and Mineral Research.
SOD2, SIRT3, OSTEOCLAST, RANKL, ROS
© 2017 American Society for Bone and Mineral Research
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
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