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. 2023 Jun 26;13(11):3826–3843. doi: 10.7150/thno.82543

Figure 5.

Figure 5

miR-24-3p loss abolishes and agomiR-24-3p reproduces the RMST knockdown-mediated effects on CF fibrogenesis. (A) TGF-β1-treated CFs were transfected with miR-24-3p NC (10 nM), antagomiR-24-3p (20 nM), or agomiR-24-3p (10 nM) with or without the knockdown of RMST. CF without any treatment served as a control. (B) Quantification of miR-24-3p expression by qRT-PCR under the different treatments. (C) CFs were immunofluorescently stained for vimentin and Ki67, and nuclei were counterstained with DAPI. Scale bar = 100 μm. (D) Quantification of Ki67-positive CFs. (E-F) The mRNA expression of (E) Ccnd1 and (F) Cdk1 in CFs was detected by qRT-PCR. (G) CFs were immunofluorescently stained for α-SMA and vimentin, and nuclei were counterstained with DAPI. (H) Quantification of α-SMA-positive cells in CFs. Scale bar = 100 μm. (I-K) The mRNA expression of (I) Col1a1, (J) Col3a1, and (K) fibronectin in CFs was detected by qRT-PCR. n = 4 to 5 independent experiments. Significance was evaluated via one-way ANOVA with the post-hoc Bonferroni test. **P < 0.01.