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. 2021 Jan 7;12:38. doi: 10.1186/s13287-020-02084-w

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© The Author(s) 2021

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 — a Immunofluorescent staining of senescent markers (P19, P53 and P16) of isolated TDSCs from control and Botox tendon showed increased accumulation of P19 and P53 in the Botox group. But P16 was not significantly changed between both groups. b Western blot of protein expression of P19 and P53 from isolated TDSCs were normalised to beta-actin and showed increased translational level of P19 and P53 in the Botox group. Results were quantified by greyscale density (n = 3; mean ± SD; *p < 0.05, **p < 0.005). c Immunofluorescence staining of P19, P53 and P16 on tendon tissue exhibited higher production of P19 and P53 in the Botox group and again not P16. d Quantification of fluorescence density of P19, P53 and P16 in tendon tissue. Blinded analysis was performed for quantification (n = 3; mean ± SD; *p < 0.05, **p < 0.005)

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