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. 2017 Apr 21;7:46649. doi: 10.1038/srep46649

Figure 3. HGF/c-Met signaling promotes the expression of Arf6 mRNA in the wounded skin.

Figure 3

(A) Eight weeks old wild type of mice were treated without (control) or with EGF, bFGF, HGF or KGF. After 1 day (upper panels) and 3 days (lower panels) of treatment, dorsal skin sections were prepared and hybridized with an antisense probe1 for Arf6 mRNA. (B,C) Signal intensity of Arf6 mRNA at 1 day (B) and 3 days (C) after treatment were measured. (D–G) Dorsal skins of 8 weeks old wild type mice were wounded and treated with inhibitors specific to EGFR, FGFR and c-Met (PD153035, SU5402 and PHA665752, respectively) at the indicated doses for 2 days, and hybridized with an antisense probe1 for Arf6 mRNA (D). Signal intensity of Arf6 mRNA at the wounded skin treated without or with PD153035 (E), SU5402 (F) and PHA665752 (G) were measured. (H) Arf6 mRNA levels in primary cultured keratinocytes treated without or with 50 ng/ml of HGF in the presence or absence of 0.5 μM of PHA665752 were analyzed by qPCR. Data show the means ± SEM from three (B–G) and five independent experiments (H). Statistical significance was assessed using one-way ANOVA with Dunnett’s multiple comparison test (B,C,E,F,G) and Tukey’s HSD test (H); *P < 0.05, n.s., not significant. Scale bar, 100 μm. Dotted lines delineate the border between epidermis and dermis.