<i>In vivo</i> overexpression of GR and GR-TR in keratinocytes delays wound healing with different kinetics of repair.

<p>A) Similar transgene expression in K5-GR and K5-GR-TR mice. Relative protein levels of the transgene <i>vs</i> endogenous GR were determined by immunoblotting using an antibody that recognizes both mouse (endogenous) and rat (transgene) GR. Actin was used as a loading control. A representative panel of three independent experiments and quantitation of three independent experiments is shown. Statistical significance was assessed by ANOVA (**<i>p</i><0.01). B) Macroscopic changes in full-thickness cutaneous wounds. The wound sites were photographed at the time indicated after wounding. Representative results from 12 mice of each genotype are shown. C) The percentage of wound closure area at each time point was estimated relative to the original wound area. Values represent mean ± SD (<i>n</i> = 12 for all groups). Statistical significance was determined using ANOVA (*<i>p</i><0.05, **<i>p</i><0.01). D) Histological evaluation of skin wounds in WT, K5-GR and K5-GR-TR mice at d4 and 8 after injury. Arrowheads and arrows indicate original wound edges and re-epithelialized edges, respectively. Trichrome staining shows distinct collagen deposition in the dermis at d8 in the indicated genotypes. Immunostaining using an anti-GR specific antibody shows GR expression and localization in WT <i>vs</i> transgenic mice (IH: GR). Note the nuclear localization of GR in both transgenic skin samples. Hematoxylin/eosin and Trichrome staining, Bars: 100 µm; IH: GR, Bar: 50 µm. E) The percentage of re-epithelialization was evaluated in WT, K5-GR and K5-GR-TR mice at d4 and d8 after wounding. All values represent the mean ±SD (<i>n</i> = 12 for all groups). Statistical significance was estimated using ANOVA (*<i>p</i><0.05, **<i>p</i><0.01).