Figure 3.

PKC activation exacerbates DLX3cKO epidermal hyperproliferation. (a) Schematic representation of TPA treatment of WT or DLX3cKO mice. (b) Hematoxylin and eosin staining of TPA-treated WT or DLX3cKO transgenic skin. Scale bar, 20 μm. Epidermal thickness was measured and data are presented as mean±S.D. of three different areas from three different mice for each condition. ***P<0.001. (c) Immunohistochemical staining of TPA-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 TPA 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 different areas from three independent mice for each condition. **P<0.01. (d) Immunohistochemical staining of TPA-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 +/− TPA. Data are presented as mean±S.D. of three different areas from three different mice for each condition. (e) Immunohistochemical staining of TPA-treated WT and DLX3cKO mice with antibodies against P-PKCα. Nuclei were stained with DAPI. Scale bar, 20 μm