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. 2018 Sep 11;6:28. doi: 10.1038/s41413-018-0028-5

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© The Author(s) 2018

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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Fig. 3 — Ssc-mir-133b/Mcl-1 mediated endogenous mitochondria-related apoptotic processes in premolar mesenchymal cells. a Mitochondrial Δψm measured by the JC-1 probe. Distribution of JC-1 aggregates (PE channel) and monomers (FITC channel) was determined by flow cytometry. b Statistical analysis of the flow cytometry results. ***P < 0.001. c Representative images show JC-1 aggregates, JC-1 monomers and merged images of both. Increases in JC-1 monomers in cells are shown in cells transfected with miR-133b. Decreased JC-1 monomers in cells are shown in cells transfected with miR-133b along with Mcl-1. Scale bar = 50 μm. d Western blotting of endogenous mitochondria-related apoptotic markers after miR-133b transfection and Mcl-1 overexpression. ***P < 0.001. e Quantitative representation of caspase-3 activity in premolar mesenchymal cells. **P < 0.01 and ***P < 0.001