The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes

• Published in: Mediators of inflammation Vol. 2017; no. 2017; pp. 1 - 8
• Main Authors: Rademacher, Franziska, Gläser, Regine, Harder, Jürgen, Cremer, Jochen, Pufe, T., Klüter, Tim, Behrendt, Peter, Lippross, Sebastian, Tohidnezhad, Mersedeh, Lammel, Justus, Bayer, Andreas, Jahr, Holger
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017; Hindawi; Hindawi Limited; Wiley
• Subjects: Analysis; Anti-Infective Agents - pharmacology; Antimicrobial activity; Antimicrobial agents; Antimicrobial peptides; beta-Defensins - metabolism; Biofilms; Blood Platelets - metabolism; Cell adhesion & migration; Cell culture; Cells, Cultured; Chemokines; Cytokines; Diabetes; Epidermal growth factor; Epidermal growth factor receptors; Fibrin; Gene expression; Growth factors; HBD-3 gene; Health aspects; Hospitals; Humans; Immunology; Intercellular Signaling Peptides and Proteins - metabolism; Intercellular Signaling Peptides and Proteins - pharmacology; Keratinocytes; Keratinocytes - drug effects; Keratinocytes - metabolism; Lysates; Peptides; Physiological research; Platelet-derived growth factor; Platelets; Real-Time Polymerase Chain Reaction; Skin; Skin - cytology; Ultrasonic imaging; Wound healing; Aachen Germany; Germany
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2017/6157491

Platelet-released growth factors (PRGF) and its related clinically used formulations (e.g., Vivostat Platelet-Rich Fibrin (PRF®)) contain a variety of chemokines, cytokines, and growth factors and are therefore used to support healing of chronic, hard-to-heal, or infected wounds. Human beta-defensin-3 (hBD-3) is an antimicrobial peptide inducibly expressed in human keratinocytes especially upon wounding. The potent antimicrobial activity of hBD-3 together with its wound closure-promoting activities suggests that hBD-3 may play a crucial role in wound healing. Therefore, we analyzed the influence of PRGF on hBD-3 expression in human primary keratinocytes in vitro. In addition, we investigated the influence of Vivostat PRF on hBD-3 expression in artificially generated human skin wounds in vivo. PRGF treatment of primary keratinocytes induced a significant, concentration- and time-dependent increase in hBD-3 gene expression which was partially mediated by the epidermal growth factor receptor (EGFR). In line with these cell culture data, in vivo experiments revealed an enhanced hBD-3 expression in experimentally produced human wounds after the treatment with Vivostat PRF. Thus, the induction of hBD-3 may contribute to the beneficial effects of thrombocyte concentrate lysates in the treatment of chronic or infected wounds.