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. 2021 May 20;12:294. doi: 10.1186/s13287-021-02358-x

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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. 6 — Upregulation of Cav1 after hPMSCs treatment was important in relieving liver fibrosis and inhibition of activated HSCs. a Immunohistochemistry staining using anti CAV1 antibody in liver sections. b Immunofluorescence staining using anti CAV1 antibody in HSCs. c, d Expression of fibrosis-related genes (c) and TGF-/Smad signaling pathway related genes (d) at different groups was determined using qRT-PCR. Relative mRNA expression was normalized to -actin and compared with the NC group. Cells from blank group were unactivated HSCs, cells from si (1-3) group or NC group were HSCs that transfected with Cav1 siRNA (1-3) or Cav1 siRNA-negative control. Scale bar, 50 m. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05; ns, no significance