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. 2020 Jun 11;33(4):1006–1016. doi: 10.1007/s13577-020-00387-x

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© The Author(s) 2020

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/.

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Fig. 5 — HDAC inhibition disrupts TGF-β/Smad Signaling by miR-15 and miR-16 to protect against pancreatic fibrosis. a The protein levels and the related quantification of α-SMA, SMAD5 and SMAD7 in PSCs after overexpression of miR-15 or miR-16. b Immunofluorescence staining of α-SMA in PSCs after overexpression of miR-15 or miR-16. c The protein levels and the related quantification of α-SMA, SMAD5 and SMAD7 in PSCs after transfected with miR-15 inhibitor or miR-16 inhibitor with or without SAHA. All data are presented as the mean ± S.D. (n = 3). ***P < 0.001, compared with control. Each assay was performed in triplicate