Figure 3.

Epidermal keratinocytes migrate over the wound bed to epithelialize the wound gap. Immunofluorescence staining with keratin 17 (K17, red) antibody demonstrates epithelialization process in human ex vivo wound model. White arrows indicate wound edges after initial wounding, while yellow arrows point at the edges of the migrating epithelial fronts. K17 is not present at the time of wounding (0 h, A). Immediately after injury (A), keratinocytes release proinflammatory cytokines and growth factors, including interleukin 1 (IL-1), tumor necrosis factor α (TNFα), and epidermal growth factor (EGF). In response to these stimuli, keratinocytes become activated and start migrating over the wound bed. Migrating keratinocytes show an upregulation of K17 (48 h, B). Strong K17 staining persisted over 4 days after the wounding when the wound is completely closed (96 h, C). A well-balanced communication with other cell types, fibroblasts, neutrophils, endothelial cells, monocytes, and macrophages (schematically presented at the bottom), B) through various cytokines and growth factors (KGF, PDGF-bb, VEGF, GM-CSF, TGFβ, IL-8), is necessary for successful epithelialization. Nuclei are visualized with DAPI (blue). White dashed lines indicate the dermal–epidermal boundary. KGF, keratinocyte growth factor; PDGF-bb, platelet-derived growth factor bb; VEGF, vascular endothelial growth factor; TGFβ, transforming growth factor β; GM-CSF, granulocyte–macrophage colony-stimulating factor; IL-8, interleukin 8. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/wound