Abstract

Graphical Keratinocytes, as the most dominant cell type in the epidermis, play multiple roles in skin wound healing. In addition to the activation of fibrobalsts, studies have shown that Pt5-1c can facilitate the wound healing process by stimulating the migration and proliferation of keratinocyte. The underlying mechanisms of these processes is the activation of downstream EGFR signaling. Keratinocytes, as the most dominant cell type in the epidermis, play multiple roles in skin wound healing. Recently, we have shown that a short antimicrobial peptide Pt5-1c can promote skin wound healing via enhancing fibroblast proliferation and migration in vitro , and accelerating re-epithelialization of murine dermal wounds in vivo . [1] However, its effects on keratinocytes is unknown. Here we clearly showed that Pt5-1c markedly enhanced keratinocyte migration and proliferation. Moreover, Pt5-1c stimulated keratinocyte activation by inducing the phosphorylation of epidermal growth factor receptor (EGFR), Akt, extracellular signal-regulated kinase (ERK), p38, and signal transducer and activator of transcription 3 (STAT3) in keratinocytes. Importantly, Pt5-1c also increased collagen production, stimulated cell proliferation, and enhanced the phosphorylation of Akt, p38 and STAT3 in the wound skin tissues. These together indicate that Pt5-1c can promote keratinocyte migration and proliferation via activation of EGFR-mediated Akt, MAPK, and STAT3 pathways, thereby contributing to skin wound healing.