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. 2020 Nov 10;15:515. doi: 10.1186/s13018-020-02043-4

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — The potentiation of the JNK pathway ameliorates the stimulative role of miR-497-5p mimic on differentiation. miR-497-5p mimic + AZA-1 or miR-497-5p mimic + DMSO was delivered into MC3T3-E1 cells. a JNK pathway activity in transfected MC3T3-E1 cells. b MTT assessment of MC3T3-E1 cell viability. c Flow cytometric analysis for cell apoptosis. d RT-qPCR measurement of Bax, Bcl-2, OCN, and RUNX2 expression. e ALP staining for ALP activity. f ARS staining for mineralization. Data are presented as the mean ± SD of three replicates each. The unpaired t test was used for the comparison between the two groups (b, c, e, f); the two-way ANOVA was applied for the comparison among multiple groups (a, d). ^#p < 0.05 vs. MC3T3-E1 cells administrated with miR-497-5p mimic + DMSO