Fig. 4: Loss of Sema3A delayed cutaneous wound healing in vivo.

A Schematic representation of the wound-healing studies performed in K14-Cre^TM+;Sema3A^L/L and K14-Cre^TM-;Sema3A^L/L mice. B qRT-PCR analysis of epidermal Sema3A mRNA after tamoxifen induction. GAPDH served as control. Bars indicate the mean fold changes ± SEM relative to the control (K14-Cre^TM-;Sema3A^L/L group); n = 3. C Quantification of the wound closure area at different time points after wounding in the exp (K14-Cre^TM+;Sema3A^L/L) and con (K14-Cre^TM-;Sema3A^L/L) groups. Data are shown as means ± SEM; n = 6. D Representative macroscopic illustration of wound healing in exp and con animals at Days 0, 4, 7 and 14. E H&E-stained sections of wounds used for morphometric analysis of the percentage of wound closure (length of newly formed epithelium (NFE)/length of NFE + length of gap between edges of wound epithelium (red dotted line) × 100) and re-epithelialization (length of NFE). White asterisk (*) indicates the proliferative connective tissue in the control group. Scale bar = 200 µm. F Quantification of the percentage of Sema3A/ZEB2 + area of the epithelial and granulation tissue at different time points. G Quantification of the percentage of wound re-epithelialization at Days 7 and 14 after wounding in K14-Cre^TM+;Sema3A^L/L and K14-Cre^TM-;Sema3A^L/L wounds. Data are shown as means ± SEM; n = 6. H Comparison of the healing times (scab falling off) in the days after wounding. Data are shown as means ± SEM; n = 6. I Comparison of connective tissue in control and Sema3A cKO mice. Data are shown as means ± SEM; n = 6. J Thickness of crust after injury. Bars indicate the mean fold changes relative to con (K14-Cre^TM-;Sema3A^L/L) ± SEM; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001.