Epithelial–Mesenchymal Transition in Keloid Tissues and TGF-β1–Induced Hair Follicle Outer Root Sheath Keratinocytes
July 2015
in “
Wound repair and regeneration
”
TLDR Keloid scars may form due to changes in skin cell characteristics and specific protein signaling.
The study investigated the role of epithelial–mesenchymal transition (EMT) in keloid formation and its underlying mechanisms. Researchers examined EMT-associated markers and TGF-β1/Smad3 signaling in keloid tissues using immunohistochemistry and quantitative real-time PCR. They found a loss of the epithelial marker E-cadherin and a gain of mesenchymal markers FSP1 and vimentin, along with enhanced TGF-β1 expression and Smad3 phosphorylation. Additionally, changes in FGFR2 isoforms and decreased expression of ΔNp63 and TAp63 were observed, which may contribute to abnormal epidermis and appendages in keloids. In vitro, TGF-β1 induced EMT in hair follicle outer root sheath keratinocytes (ORSKs) and normal skin epithelial cells, with ORSKs showing more pronounced EMT changes. The findings suggested that ORSKs might play crucial roles in the EMT process in keloids, providing insights into the molecular mechanisms of keloid pathogenesis.
