TGF-β1 treatment rescues impaired wound closure in FOXO1-deleted mice. (A) Representative photographs of scalp wounds on day 4 and day 7 from K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice treated with vehicle or TGF-β1. (B) Wound-healing process was analyzed at different time points after wounding. Average wound area was presented as percentage of the wound area on day 0 (100%). (C) Hematoxylin and eosin staining of K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice wound biopsies on day 7 after wounding. Bar, 500 µm. WC, wound center; WE, wound epithelium; Normal, normal epithelium. The quantification of epithelial migration and re-epithelialization in the day-7 scalp wounds of K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice. The gap between epithelium (D), epithelial length (E), epithelial area (F), and epithelial thickness (G) was assessed by image analysis of hematoxylin and eosin–stained sections at the center of each wound. Paraffin-embedded cross sections from K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice were treated with either vehicle or TGF-β1 and were analyzed by immunofluorescence using an anti-uPAR antibody and anti-PCNA antibody. Percentage of uPAR-positive migrating keratinocytes was quantified in normal and wound epithelium (H) as well as in hair follicles (I). (J) PCNA-positive proliferative keratinocytes in wound epithelium. EP, epidermis; CT, connective tissues; *, P < 0.05. Error bars represent mean ± SEM, n = 4–6 mice per group.