Platelet-Released Growth Factors Induce Expression of Genes Involved in Extracellular Matrix Organization and Epidermis Development in Primary Human Keratinocytes and Fibroblasts
Platelet-released growth factors (PRGF) is a thrombocyte concentrate lysate. Similar to its clinically equivalent variations (e.g. Vivostat PRF), it is widely known to be able to support the healing of chronic and hard-to-heal wounds. However, the exact mechanisms of action of PRGF are not completely known. Therefore, this study investigated the working mechanisms of PRGF through the identification of genes in keratinocytes and fibroblasts influenced by PRGF.
Whole transcriptome analysis and gene ontology (GO) enrichment of PRGF-stimulated keratinocytes revealed an increased expression of genes involved in extracellular matrix organization. This study particularly focused on transforming growth factor beta-induced (TGFBI), fibronectin 1 (FN1), matrix metalloprotease 9 (MMP9), transglutaminase 2 (TGM2), collagen type XXII alpha 1 chain (COL22A1), fermitin family member 1 (FERMT1), collagen type I alpha 1 chain (COL1A1), collagen type II alpha 2 chain (COL1A2) and Keratin 7 (KRT7). Real-time polymerase chain reaction (PCR) confirmed the in-vitro PRGF-mediated induction of the selected genes in keratinocytes and revealed induction of these genes in fibroblasts. TGFBI, FN1, MMP9, FERMT1 and COL1A2 were further induced by PRGF in an ex vivo setting. Additionally, PRGF promotes Ki67 and Vascular endothelial growth factor A (VEGFA) expressions in fibroblasts in vitro, indicating support of angiogenesis and fibroblast proliferation. A scratch assay further shows that PRGF increases fibroblast migration in vitro. Overall, this study has demonstrated that PRGF influence on extracellular matrix organization in keratinocytes and fibroblasts may be a significant factor of its wound healing capabilities. Additionally, PRGF may support wound healing by promoting cell adhesion, cornification and fibroblast proliferation.
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