SIRT1 suppresses high glucose and palmitate-induced osteoclast differentiation via deacetylating p66Shc
作者： Bo Qu , Kai Gong , Hongsheng Yang , Yugang Li , Tao Jiang
DOI: 10.1016/J.MCE.2018.02.015
关键词:
摘要: Abstract Findings concerning the role of diabetes mellitus (DM) in osteoclast differentiation are contradictory in vivo and in vitro. Sirtuin 1 (SIRT1) can inhibit RANKL-induced osteoclastogenesis deacetylate p66Shc suppress its phosphorylation high glucose (HG)-stimulated human umbilical vein endothelial cells. This study aimed to investigate mechanism SIRT1 DM-related differentiation. Osteoclast precursors were cultured with HG palmitate (PA), or without resveratrol/sirtinol. TRAP staining was used evaluate formation. The expression SIRT1, RANK, RANKL, OPG, NFATc1, TRAP, c-fos, p66Shc, phospho-p66Shc (S36), phospho-NF-κBp65 (p-p65), IκB determined by real-time PCR western blotting. Lysine acetylation assayed immunoprecipitation. Reactive oxygen species (ROS) production analyzed DCFH-DA fluorescence. siRNA PDTC confirm osteoclastogenesis. We found PA enhanced differentiation, decreased OPG expression, increased levels c-fos. Upregulation resveratrol inhibited HG- PA-induced whereas sirtinol further it. Resveratrol suppressed lysine S36 ROS production, NF-κB activation induced PA, while boosted these processes. abrogated activation. In addition, greatly RANK RANKL PA. conclusion, this confirms DM suppresses via p66Shc/ROS/NF-κB signaling.
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