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Skin wound healing is a complex, multi-step process that encompasses various cells, growth factors, cytokines, and components of the ex-tracellular matrix (Baum and Arpey, 2005). An essential feature of a healed wound is the restoration of an intact epidermal barrier. Re-epithelialization is a key event in wound healing and is mainly achieved by keratinocyte migration, proliferation, and differentiation (Coulombe, 2003). The absence of keratino-cyte migration at the wound edge is a critical defect related to the clinical phenotype of chronic nonhealing wounds, such as diabetic ulcers (Brem and Tomic-Canic, 2007). How-ever, the exact manner in which keratinocyte migration is regulated during wound healing also remains largely unknown. The skin is an organ that displays a highly ac-tive metabolism of fatty acids, such as prostaglan-dins (PGs), HETEs (hydroxyeicosatetraenoic acids), and leukotrienes, etc. (Ziboh et al., 2000). Nu-merous studies showed that lipid mediators are involved in regulating skin inflammation (Serhan et al., 2008; Kendall and Nicolaou, 2013) related to psoriasis (Mayser et al., 2002), ichthy-osis (Yu et al., 2005), and contact dermatitis (Miki et al., 2013). Recently, ATL (aspirin-triggered 15-epi-lipoxin A4), and resolvin D1 and E1 have been reported to enhance wound healing and epithelial cell regeneration via limiting PMN (polymorphonuclear leukocyte) infiltration and directly stimulating epithelial cells (Norling et al., 2011) in many inflammation-driven diseases, such as cantharidin-induced skin blis