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. 2021 Sep 2;24(5):758. doi: 10.3892/mmr.2021.12398

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Copyright: © Yuan et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — Effects of miR-29a-modified hADSCs-exo on the TGF-β2/Smad3 signaling pathway and fibrosis of human hypertrophic scar fibroblasts. (A) Western blotting results. (B) Relative expression level of TGF-β2. (C) Relative expression level of p-Smad3. (D) Relative expression level of the fibrosis gene α-SMA. (E) Relative expression level of Col-I. (F) Relative expression level of Col-III. One-way ANOVA followed by Bonferroni post hoc test was used to compare the differences among different groups. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. NC group; ^##P<0.01, ^###P<0.001 vs. mimics-exo group; ^@P<0.05, ^@@P<0.01 vs. mimics-exo + SRI-011381 group. Col-I, collagen I; Col-III, collagen III; miR, microRNA; NC, negative control; α-SMA, α-smooth muscle actin; p-, phosphorylated; mimics-exo, exosomes from miR-29a overexpressed hADSCs treated group; inhibitor-exo, exosomes from miR-29a knockdown hADSCs treated group; hADSCs, human adipose-derived mesenchymal stem cells.