Li, J.Cao, J.Li, M.Yu, Y.Yang, Y.Xiao, X.Wu, Z.Wang, L.Tu, Y.Chen, H.2025-12-182025-12-182011British Journal of Dermatology, 2011; 164(5):1030-10360007-0963https://hdl.handle.net/11541.2/138192Background: Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. There is evidence that transforming growth factor (TGF)-β is involved in keloid formation. Collagen triple helix repeat containing-1 (Cthrc1) was identified as a novel gene expressed in the adventitia and neointima on arterial injury. It is indicated to be a cell type-specific inhibitor of TGF-β, which functionally increases cell migration while reducing collagen type I and III deposition. However, to our knowledge expression and regulatory mechanisms of Cthrc1 and TGF-β1 in keloid and normal skin have not been studied before. Objectives: Cthrc1 gene regulation and potential role in keloid formation were determined, and its correlation with TGF-β1 involved in keloid pathogenesis was examined in human fibroblasts of keloids and normal skin. Methods: The expression of Cthrc1 and TGF-β1 was investigated in fibroblasts of keloid and normal skin. Collagen type I expression and collagen synthesis in keloid fibroblasts induced by TGF-β1 were examined. Then, recombinant Cthrc1 was applied to assess its correlation with TGF-β1. Results: Increased TGF-β1 and Cthrc1 expression was examined in keloid compared with normal skin. Cthrc1 expression increased in a concentration-dependent manner induced by TGF-β1 in keloid fibroblasts. TGF-β1 stimulated collagen type I expression and collagen synthesis in keloid fibroblasts, which can be reversed by recombinant Cthrc1. Conclusions: TGF-β1 was upregulated in keloid fibroblasts and recombinant Cthrc1 inhibited TGF-β1-stimulated collagen type I synthesis, which suggests that Cthrc1 may be a potential therapeutic option for keloids.enCopyright 2011 The Authorshidradenitis suppurativa lesionsprostaglandin e-2 productionacne inversahuman skinstereologyultrasoundinfliximabsebocytesbacteriareceptorJournal article10.1111/j.1365-2133.2011.10215.x2-s2.0-79955370589