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. 2019 Jan 29;9:878. doi: 10.1038/s41598-018-37027-2

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Activation of SIRT1 relives RUNX2 and Osteocalcin activation. (a) RUNX2 mRNA significantly decreased via SRT1720 activation and significantly increased via Sirtinol treatment (n = 4–9). (b) Acetylation of RUNX2 promoter region was determined via chromatin immunoprecipitation. RUNX2 promotor acetylation was significantly reduced with SRT1720 activation (n = 3). (c) RUNX2 protein was significantly decreased via SRT1720 activation and significantly increased via Sirtinol treatment (n = 3). (d) OCN activity measured via fluorescence increased in hyperglycaemic conditions compared to osteogenic, with SIRT1 activator attenuating this process and SIRT1 inhibitor Sirtinol increasing OCN fluorescence (n = 4 and 5FoV), OCN mRNA followed a similar pattern, with a decrease in OCN transcripts in SRT1720 activated cells (n = 4–9). *P < 0.05, **P < 0.005, ***P < 0.001. Scale Bars = 10 μm.