Accelerated wound closure upon epidermal <i>Pten</i> deletion: Enhanced mTor activation and re-epithelization.

<p>(A) Representative example of accelerated wound closure in <i>Pten-</i>deficient (K14Cre <i>Pten</i>^F/F) mice compared to control mice 4 days after skin wounding. (B) Quantification of the wound area is represented by the box-and-whiskers graphic (horizontal line, median value; <i>n</i> = 13 for each group; **p = 0.0071). (C) Percentage of mice exhibiting open wounds after surgical incision in control mice (triangles, n = 8) and K14Cre <i>Pten</i>^F/F mice (squares, n = 8) at the indicated days is depicted. There was a significant increase in the rate of wound closure (***p<0.0001). (D) Representative examples of K10 and K14 (red-upper panel), pAkt⁴⁷³ (red-middle panel), and pS6 (red–lower panel) expression in K14Cre <i>Pten</i>^F/F wounds as determined by immunofluorescence. DAPI (blue) and fibrin(ogen) (green). Note the accumulation of pAkt⁴⁷³ and pS6 in the transitional zone and epithelial tongue at the wound edge (transitional and epithelial tongue), when compared to the adjacent epithelium (Normal). (E) Quantification of BrDU positive cells in histological slides at the transitional and wound edge of control and K14Cre <i>Pten</i>^F/F mice (<i>n</i> = 10 for each group; *p = 0.0331). (F) Quantification of epithelial migration and re-epithelization. The length of the epithelial tongue was measured in histological slides of wounded control (n = 10) and K14Cre <i>Pten</i>^F/F mice (n = 12) (mean; *p = 0.0268).