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. 2017 Apr 6;7:672. doi: 10.1038/s41598-017-00796-3

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© The Author(s) 2017

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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Overexpression of SIRT3 enhanced SOD2 expression through the interaction with FoxO3a in NaF-treated TCMK-1 cells. TCMK-1 cells were transfected with SIRT3 expression constructs (WT or N87A) followed by exposure to NaF (3 mM) for 12 h. (a) Mitochondrial fractions were immunoprecipitated with polyclonal antibodies against FoxO3a. Interaction of endogenous SIRT3 and FoxO3a was detected by immunoblotting analysis. (b) The expression of phosphorylated FoxO3a was determined by immunocytochemistry using a fluorescence microscope (magnification, × 100). (c) FoxO3a acetylation at lysine-100 residue was examined using CO-IP analysis. (d) Nuclear location of FoxO3a was measured. (e) Expressions of FoxO3a and SOD2 were examined in mitochondrial fraction. (f) ChIP analysis was used to examine the binding of FoxO3a to the SOD2 promoter. All results are presented as means ± s.d. of at least three independent experiments. ^*p < 0.05, ^**p < 0.01 versus scramble group, ^##p < 0.01 versus the NaF + scramble group, ^$$p < 0.01 versus the NaF + SIRT3 group. Full-length blots/gels are presented in Supplementary Figures S15 and 16.