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Fig. 4 | BMC Genomics

Fig. 4

From: Inhibition of CUB and sushi multiple domains 1 (CSMD1) expression by miRNA-190a-3p enhances hypertrophic scar-derived fibroblast migration in vitro

Fig. 4

The overexpression/ knockdown of miR-190a-3p promoted/ inhibited cell migration and FN1 secretion in fibroblasts. (A, E) Transwell assay was performed to detect the migratory ability of the miR-190a-3p mimics-treated fibroblasts and was compared to negative control. Quantification of numbers of migrated cells per field was presented as mean ± SD from three independent experiments in panel E. Scale bar: 200 μm, ***p < 0.001. (B, F) Wound healing assay was performed to detect the migratory ability of the miR-190a-3p mimics-treated fibroblasts and was compared to negative control. The wound area at 0 h was set as 100%. Quantification of the healing rate from the three independent experiments in panel F was shown as mean ± SD. Scale bar: 200 μm, *p < 0.05. (C, G) Transwell assay was performed to detect the migratory ability of the miR-190a-3p inhibitors-treated fibroblasts and was compared to negative control. Quantification of numbers of migrated cells per field from three independent experiments in panel G was presented as mean ± SD. Scale bar: 200 μm, **p < 0.01. (D, H) Wound healing assay was performed to detect the migratory ability of miR-190a-3p mimics-treated fibroblasts and was compared to negative control. The wound area at 0 h was set as 100%. Quantification of the healing rate from three independent experiments in panel H was shown as mean ± SD. Scale bar: 200 μm, **p < 0.01. (I-L) qRT-PCR and western blot were performed to measure the ACTA2, COL1 and FN1 mRNA and protein levels in the mimics and inhibitors group. The results showed significantly upregulated ACTA2, COL1 and FN1 mRNA levels in the miR-190a-3p mimics group, while only increased expression of FN1 at the protein level; An opposite phenomenon was observed in the inhibitors group. *p < 0.05, **p < 0.01, ***p < 0.001

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