FIGURE 5.

The FGF10‐dependent response to UVB‐induced skin injury requires YAP activity. (A) Immunofluorescence staining of Ki‐67 (Red) in untreated or UVB treated HaCat with or without FGF10 treatment in the presence or absence of si‐YAP. Nuclei were stained with DAPI (blue) (n = 3). Scale bars = 100 μm. (B) Quantification the percentage of Ki‐67‐positive cells from (A). (C) The expression of YAP and PCNA was measured by immunoblotting assay in untreated or UVB treated HaCaT with FGF10 or without FGF10 treatment in the presence or absence of si‐YAP. β‐Actin was used as a loading control (n = 3). (D,E) Quantification of YAP, PCNA protein levels in (C). (F) Representative HE staining of AAV‐GFP or AAV‐Fgf10 transfected skin treated with or without UVB in the presence or absence of VP (n = 3). Scale bars = 100 μm. (H) Quantification the epidermal thickness from (F). (G) Immunohistochemical staining of PCNA in the AAV‐GFP or AAV‐Fgf10 transfected skin treated with or without UVB in the presence or absence of VP. The positive staining (brown) demonstrated positive expression (n = 3). Scale bars = 100 μm. (I) Quantification the epidermal thickness from (G). The data are presented as the means ± SEM. ***P < 0.001, **P < 0.01, *P < 0.05, ^### P < 0.001, ^## P < 0.01, ^&& P < 0.01, ^& P < 0.05 vs. the corresponding control siRNA HaCaT group