Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이수영 | * |
dc.contributor.author | 김현석 | * |
dc.contributor.author | 허정은 | * |
dc.date.accessioned | 2016-08-29T12:08:05Z | - |
dc.date.available | 2016-08-29T12:08:05Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 2045-2322 | * |
dc.identifier.other | OAK-16523 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/231107 | - |
dc.description.abstract | The mitochondrial sirtuin 3 (SIRT3) is involved in suppressing the onset of multiple pathologies, including cardiovascular disease, fatty liver, age-related hearing loss, and breast cancer. But a physiological role of SIRT3 in bone metabolism is not known. Here we show that SIRT3 is a key regulatory molecule to maintain bone homeostasis. Mice deficient in SIRT3 exhibited severe osteopenia owing to increased numbers of osteoclasts. Osteoclast precursors from Sirt3-/- mice underwent increased osteoclastogenesis in response to receptor activator of nuclear factor-κB ligand (RANKL), an essential cytokine for osteoclast differentiation. SIRT3 expression from RANKL induction depended on the transcription coactivator PGC-1β (peroxisome proliferator-activated receptor-γ co-activator-1β) and the nuclear receptor ERRα (estrogen receptor-related receptor α), and that SIRT3 inhibited the differentiation by interfering with the RANKL-induced expression of PGC-1β. Thus an auto-regulatory feedback mechanism operates to induce its own inhibitor SIRT3 by PGC-1β. Moreover, Sirt3-/- osteoclast precursors reduced AMP-activated protein kinase (AMPK) phosphorylation through down-regulating the expression of AMPK. Our results suggest that a mitochondrial SIRT3 is an intrinsic inhibitor for RANKL-mediated osteoclastogenesis. | * |
dc.language | English | * |
dc.publisher | Nature Publishing Group | * |
dc.title | Sirtuin 3 (SIRT3) maintains bone homeostasis by regulating AMPK-PGC-1β axis in mice | * |
dc.type | Article | * |
dc.relation.volume | 6 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Scientific Reports | * |
dc.identifier.doi | 10.1038/srep22511 | * |
dc.identifier.wosid | WOS:000371059200001 | * |
dc.identifier.scopusid | 2-s2.0-84959461324 | * |
dc.author.google | Huh J.-E. | * |
dc.author.google | Shin J.H. | * |
dc.author.google | Jang E.S. | * |
dc.author.google | Park S.J. | * |
dc.author.google | Park D.R. | * |
dc.author.google | Ko R. | * |
dc.author.google | Seo D.-H. | * |
dc.author.google | Kim H.-S. | * |
dc.author.google | Lee S.H. | * |
dc.author.google | Choi Y. | * |
dc.author.google | Kim H.S. | * |
dc.author.google | Lee S.Y. | * |
dc.contributor.scopusid | 이수영(53980218900;7409697278) | * |
dc.contributor.scopusid | 김현석(57191717681) | * |
dc.contributor.scopusid | 허정은(57220704929) | * |
dc.date.modifydate | 20240415140424 | * |