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. 2017 Feb 10;24(4):717–730. doi: 10.1038/cdd.2017.5

Figure 5.

Figure 5

PKC inhibition partially restores epidermal thickness and keratinocyte proliferation in DLX3cKO skin. (a) Schematic representation of GF109203X (GF) treatment of WT or DLX3cKO mice. (b) H&E staining of GF-treated WT and DLX3cKO skin. Epidermal thickness was measured and data are presented as mean±S.D. of three different areas from three different mice per condition. (c) Immunohistochemical staining of GF-treated WT and DLX3cKO transgenic skin with antibodies against Ki-67. Nuclei were stained with DAPI. Scale bar, 20 μm. Bottom panel, Ki-67-positive cell count in WT and DLX3cKO epidermis +/− GF. Data are presented as mean±S.D. of three different areas from three different mice for each condition. (d) Immunohistochemical staining of GF-treated WT and DLX3cKO transgenic skin with antibodies against KRT5 and DLX3. Nuclei were stained with DAPI. Scale bar, 20 μm. Bottom panel, bar graph showing the number of DLX3-positive cells normalized versus the nuclei in WT and DLX3cKO skin treated with GF or acetone (control). DLX3-positive cells and the number of nuclei in each section were determined by ImageJ software analysis of the labeled particles. Data are presented as mean±S.D. of three separate areas from three different mice for each condition. ***P<0.001. (e) Immunohistochemical staining of GF-treated WT and DLX3cKO mice with antibodies against P-PKCα and (f) against KRT5 and KRT10 (upper panel) and Filaggrin (lower panel). Nuclei were stained with DAPI. Scale bar, 20 μm. (g) Total ERK and phosphor-ERK (P-ERK) expression levels determined by western blot of protein extracts from GF-treated WT and DLX3cKO transgenic skin. GAPDH was used as a loading control