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Mediators of Inflammation
Volume 2017, Article ID 6157491, 8 pages
Research Article

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

1Department of Heart and Vascular Surgery, University Hospital of Schleswig-Holstein, Campus Kiel, Arnold-Heller Straße 3, Haus 26, 24105 Kiel, Germany
2Department of Dermatology, University Hospital of Schleswig-Holstein, Campus Kiel, Schittenhelmstr. 7, 24105 Kiel, Germany
3Institute of Anatomy and Cell Biology, RWTH University of Aachen, Wendlingweg 2, 52072 Aachen, Germany
4Department of Traumatology, University Hospital of Schleswig-Holstein, Campus Kiel, Arnold-Heller Straße 3, Haus 18, 24105 Kiel, Germany
5Department of Orthopaedics, Aachen University Hospital, Pauwelsstraße 30, 52074 Aachen, Germany

Correspondence should be addressed to Andreas Bayer; ed.bew@leik-reyabsaerdna

Received 19 January 2017; Accepted 6 July 2017; Published 25 July 2017

Academic Editor: Vinod K. Mishra

Copyright © 2017 Andreas Bayer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.