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Platelet‐released growth factors induce the antimicrobial peptide human beta‐defensin‐2 in primary keratinocytes
Author(s) -
Bayer Andreas,
Lammel Justus,
Rademacher Franziska,
Groß Justus,
Siggelkow Markus,
Lippross Sebastian,
Klüter Tim,
Varoga Deike,
Tohidnezhad Mersedeh,
Pufe Thomas,
Cremer Jochen,
Gläser Regine,
Harder Jürgen
Publication year - 2016
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12966
Subject(s) - beta defensin , antimicrobial peptides , platelet , platelet rich fibrin , in vivo , wound healing , defensin , biology , peptide , pharmacology , microbiology and biotechnology , fibrin , chemistry , antimicrobial , immunology , biochemistry
Platelet‐released growth factors ( PRGF ) and its related clinically used formulations [e.g. Vivostat platelet‐rich fibrin ( PRF ® )] are thrombocyte concentrate lysates that support healing of chronic, hard‐to‐heal and infected wounds. Human beta‐defensin‐2 ( hBD ‐2) is an antimicrobial peptide expressed in human keratinocytes exhibiting potent antimicrobial activity against wound‐related bacteria. In this study, we analysed the influence of PRGF on hBD ‐2 expression in human primary keratinocytes and the influence of Vivostat PRF ® on hBD ‐2 expression in experimentally generated skin wounds in vivo . Treatment of primary keratinocytes with PRGF caused a significant increase in hBD ‐2 gene and protein expressions in a concentration‐ and time‐dependent manner. The use of blocking antibodies revealed that the PRGF ‐mediated hBD ‐2 induction was partially mediated by the epidermal growth factor receptor and the interleukin‐6 receptor ( IL ‐6R). Luciferase gene reporter assays indicated that the hBD ‐2 induction through PRGF required activation of the transcription factor activator protein 1 ( AP ‐1), but not of NF ‐kappaB. In concordance with these cell culture data, Vivostat PRF ® induced hBD ‐2 expression when applied to experimentally generated skin wounds. Together, our results indicate that the induction of hBD ‐2 by thrombocyte concentrate lysates can contribute to the observed beneficial effects in the treatment of chronic and infected wounds.