The role of stem cell factor and c-KIT in keloid pathogenesis: do tyrosine kinase inhibitors have a potential therapeutic role?

摘要: Summary Background  Keloids are fibroproliferative disorders characterized by increased deposition of extracellular matrix components. Stem cell factor (SCF) and its receptor c-KIT expressed in a wide variety cells have also been demonstrated to be important modulators the wound healing process. Objectives  To examine role SCF/c-KIT system keloid pathogenesis. Methods  Immunohistochemical staining Western blot analyses were used localization expression SCF normal skin tissue. This was followed detection fibroblasts cultured vitro exposed serum. investigate effect epithelial–mesenchymal interactions, two-chamber employed which keratinocytes on membrane inserts cocultured with fibroblasts. levels all extracts conditioned media assayed blotting. In another set experiments, imatinib (Glivec®, Gleevec®; Novartis Pharma AG, Basel, Switzerland) examined. Results  upregulated scar tissue stimulated serum, highlighting their importance initial phase healing. We further that mimicked coculture vitro, not only secretion soluble form cocultures but brought about shedding domain perhaps upregulation tumour necrosis factor-α converting enzyme scars vivo vitro. addition phosphorylated an activation system. Finally, we imatinib, tyrosine kinase inhibitor, may possible therapeutic agent for keloids. Conclusion  These data indicate plays pathogenesis, underscore as key scars.