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. 2022 Feb 23;13:80. doi: 10.1186/s13287-022-02723-4

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© The Author(s) 2022

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. 7 — miR-144-3p promoted tendon repair via targeting ARID1A in tenocytes. A ARID1A was predicted as a potential target of miR-144-3p by all three bioinformatic programs (TargetScan, miRDB and DIANA TOOLS). B Plasmid vectors of ARID1A 3′UTR and its mutation. C Dual-luciferase reporter assay showed that miR-144-3p targeted ARID1A 3′UTR but not its mutation (Bars: mean ± SE; n = 3; unpaired Student’s t test: miR-NC vs. miR-144-3p in wild type groups; miR-NC vs. miR-144-3p in mutant groups, *p < 0.05). D, E miR-144-3p mimic suppressed ARID1A mRNA and protein expression in tenocytes, while miR-144-3p inhibitor removed the suppression effects (Bars: mean ± SE; n = 3; unpaired Student’s t test: mimic-NC vs. miR-144-3p mimic; inhibitor-NC vs. miR-144-3p inhibitor, *p < 0.05 and **p < 0.01)