549 In vitro superficial and full thickness wound models to study re-epithelialization processes

Abstract

Keloids are fibroproliferative scars that invade the surrounding tissue beyond the original wound site. The cellular and molecular mechanism for the pathogenesis of keloid scars are still unknown. We investigated the role of the transcription factor Twist, a key regulator in epithelial-to-mesenchymal transition, its upstream regulators, and downstream targets, which are associated with self-renewal, proliferation and invasion, in keloid tissue. Multicolour immunofluorescence microscopy was performed on frozen tissue sections of keloid scars, normal scars and normal skin staining for Twist, and related molecules such as Bmi1, active b-catenin and inhibitor of differentiation 1 (Id1). Staining of these markers was quantified using Metamorph software. Endothelial and mesenchymal cells were identified and inflammatory infiltrates were investigated using markers for T cells, B cells, and macrophages. Our results reveal remarkable upregulation of Twist expression in keloids compared to normal scar and normal skin. Furthermore, we show a significant increase in expression of Bmi1, active