Fig. 4: TGF-β1 represses miR-200b/c-3p expression in keratinocytes.

a RT-qPCR analysis of mice dorsal skin wounds at the indicated time points showed elevated TGF-β1 expression (n = 3). b Mice dorsal skin was intradermally injected at the wound edge with TGF-β type I receptor inhibitor SB431542 (10, 20, 50, and 100 μg per mouse) or PBS as negative control. Wound edge samples were collected at 4 and 8 dpw. c Representative live images of wounds and quantitative data of wound healing rate at 0, 2, 4, 6, 8, and 10 dpw showed delayed wound healing in SB431542-injected wounds (n = 6). d Wound edge samples of 4 and 8 dpw treated as in (c) were used for H&E staining. Representative images of epithelial tongues (indicated by dashed lines) showed repression of re-epithelialization in SB431542-injected wounds. Arrows indicate wound edges. e Quantitative data of the length of epithelial tongues from samples as in (d) (n = 3). f RT-qPCR analysis of samples of 4 dpw treated with PBS or SB431542 showed elevated miR-200b/c-3p expression when TGF-β1 signaling was inhibited (n = 3). g RT-qPCR analysis of HaCaT cells treated as indicated with TGF-β1 (10 ng/ml) and SB431542 (10 nM) for 24 h (n = 3). dpw, days post-wounding. Data presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 versus control, Student’s t-test in (a, f, g), one-way ANOVA in (c, e). Scale bars: 5 mm in (c), 200 μm in (d).