Keratinocyte-specific FOXO1 deletion delays wound closure. (A) Relative fold change of FOXO1 mRNA expression levels normalized to ribosomal protein L32 mRNA expression levels in the scalp wounds of control K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice as measured by qRT-PCR. (B) FOXO1-immunostained sections (red) were counterstained with DAPI (blue). Bar, 100 µm. (C) Relative intensity measurements of FOXO1 immunostaining in the epithelium. (D) Quantification of FOXO1 nuclear localization in the wounded epithelium and normal epithelium on FOXO1-immunostained sections. (E) Representative photographs of scalp wounds on day 4 and 7 from K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice. (F) Wound-healing process was analyzed at different time points after scalp wounding. Average wound area was presented as percentage of the wound area on day 0 (100%). (G) K14.Cre⁻.FOXO1^L/L and K14.Cre⁺.FOXO1^L/L mice were stratified into three groups: (1) high degree of healing (covering >70% of the original wound surface), light bars; (2) moderate (covering 30–70%), gray bars; or (3) little to no healing (covering >30%), dark bars. EP, epidermis; CT, connective tissues; White dashed lines demarcate the epidermis from the dermis. Asterisks indicate significant increase or decrease compared with control mice (P < 0.05). Error bars represent mean ± SEM, n = 6–9 per group.