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. 2019 Dec 12;14:434. doi: 10.1186/s13018-019-1505-2

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — Knockdown of p38 suppressed the activation of p38/ERK/JNK signal pathway in TGF-β1-induced BMSCs. Western blot showed that the expression of p-p38, p-ERK, and p-JNK was remarkably increased in the BMSCs under TGF-β1 induced for 14 days, while shRNA-p38 and SB203580 suppressed the activation of p38/ERK/JNK signal pathway in TGF-β1-induced BMSCs. The non-phosphorylated proteins of p38, ERK, and JNK were essentially unchanged in different groups. **p < 0.01 and ***p < 0.001 vs. control; ^##p < 0.01 and ^###p < 0.001 vs. TGF-β1