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. 2020 Nov 3;11(11):947. doi: 10.1038/s41419-020-03155-9

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© The Author(s) 2020

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. 5 — a Effects of IL-1β on activation of TGF-β signaling in AC and SW1353 cells expressing NC or miR-18a inhibitor were assessed. b Expression of hypertrophy-related genes was analyzed in NC- or miR-18a inhibitor-expressed cells in response to IL-1β. c TGF-β signaling downstream genes expression was analyzed in IL-1β-suppressed cells with or without miR-18a re-expression. d Effects of LY2109761 on chondrocyte hypertrophy in cells with IL-1β treatment and miR-18a inhibitor expression were determined. e qRT-PCR shows the expression of hypertrophy-related genes when TGFβ1, SMAD2, or SMAD3 was restored expressed in cells with IL-1β stimulation. f Activity of NF-κB and TGF-β signaling, and expression of RUNX2 were determined in rat model of OA in Fig. 1a. Scale bar: 50 μm. g, h Activity of TGF-β signaling and the expression of hypertrophic genes in chondrocytes were assessed in cells in response to TNFα with or without inhibition of miR-18a. Data in a–c are presented as mean ± SD. *P < 0.05.