SIRT1 suppresses high glucose and palmitate-induced osteoclast differentiation via deacetylating p66Shc

Molecular and Cellular Endocrinology
Bo QuXianming Pan

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 and deacetylate p66Shc suppress its phosphorylation in high glucose (HG)-stimulated human umbilical vein endothelial cells. This study aimed to investigate the role and mechanism of SIRT1 in DM-related osteoclast differentiation. Osteoclast precursors were cultured with HG and palmitate (PA), with or without resveratrol/sirtinol. TRAP staining was used to evaluate osteoclast formation. The expression of SIRT1, RANK, RANKL, OPG, NFATc1, TRAP, c-fos, p66Shc, phospho-p66Shc (S36), phospho-NF-κBp65 (p-p65), and IκB was determined by real-time PCR or western blotting. Lysine acetylation of p66Shc was assayed by immunoprecipitation. Reactive oxygen species (ROS) production was analyzed by DCFH-DA fluorescence. p66Shc siRNA and PDTC were used to confirm the mechanism of SIRT1 in osteoclastogenesis. We found HG and PA enhanced osteoclast differentiation, decreased SIRT1 and OPG expression, and increased levels of RANK, RANKL, NFATc1, TRAP, and c-fos. Upregulation of SIRT1 by resveratrol inhibited HG- and PA-induced osteoclast differentiation, whereas ...Continue Reading

Citations

Jun 6, 2019·Basic Research in Cardiology·Kerstin BoenglerRainer Schulz
Jan 18, 2021·Annals of the New York Academy of Sciences·Kai NanKun-Zheng Wang
Jan 17, 2021·Life Sciences·Ye ChenEn Luo

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