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. 2021 Oct 5;22(19):10780. doi: 10.3390/ijms221910780

Figure 7.

Figure 7

HLSC-EVs regulate β-catenin through miR29b. (A) Expression of hsa-miR29 a, b, and c in fibroblast treated with or without (control) TGFβ1 for 24 h at 37 °C. Data represent mean ±SD of three independent experiments performed in triplicate, **** p < 0.001 control vs. TGFβ1; # p < 0.01 TGFβ1 miR29b vs. TGFβ1 mir29a and TGFβ1 miR29c. (B) Expression of hsa-miR29b in mkCF cells transfected with control siRNA or Ctnnb1 siRNA for 72 h. (C) Expression of miR29b in AAN mice experimental groups. A significant up-regulation of miR29b is observed in AAN mice treated with HLSC-EVs. * p < 0.05, (n = 5 mice per group). (D) RT-PCR showing the expression of miR29b in fibroblasts treated with TGFβ1 alone or TGFβ1 with HLSC-EVs, or with TGFβ1 with HLSC-EVs in the presence of α-Amanitin for 6 h at 37 °C. Post-experimental analysis revealed a significant reduction in miR29b following treatment with TGFβ1, which was up-regulated in the presence of HLSC-EVs. HLSC-EV treatment in the presence of α-Amanitin showed no significant increase in the expression of miR29b. **** p < 0.0001 was considered statistically significant. (E) The expression of miR29b in fibroblasts co-cultured with mTECs pre-treated with AA increased following treatment with HLSC-EVs and was significantly reduced in the presence of antimiR29b. * p < 0.05, ** p < 0.01 was considered to be statistically significant. (F) Expression of β-catenin and pro-fibrotic genes in fibroblasts co-cultured with mTECs pre-treated with AA in the presence or absence of HLSC-EVs, or HLSC-EVs together with antimiR29b, or HLSC-EVs with antimiR SCR. * p < 0.05, ** p < 0.001 were considered to be statistically significant. Data represent mean ± SD of three independent experiments.