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

Figure 4.

Figure 4

PKC activation raises the DLX3cKO epidermal barrier alteration and inflammatory phenotype. (a) Heatmaps of differentially expressed mRNAs in WT or DLX3cKO skin treated with TPA or acetone (control) represent the top affected clusters by DAVID functional annotation analysis: epidermal barrier disruption (left), cytokine/chemokine (middle) and antimicrobial peptides (right). Expression values are colored based on their z-score after normalization across treatments. (b) Immunohistochemical staining of TPA-treated WT and DLX3cKO transgenic skin with antibodies against CD45. Nuclei were stained with DAPI. Scale bar, 20 μm. (c) Heatmap of the cytokines released by WT or DLX3cKO keratinocytes after treatment with TPA in culture for 24 h. DMSO was used as a control. Cytokine concentration values are colored based on their z-score after normalization across treatments. (d) Bar graph showing GO term Biological Process (BP) enrichment by DAVID Functional Annotation tool in DLX3cKO versus WT keratinocytes treated with TPA for 36 h. (e) Bar graph showing the fold change for keratinocyte differentiation-related genes in TPA-treated DLX3cKO versus WT keratinocytes