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Collagen triple helix repeat containing-1 inhibits transforming growth factor-β1-induced collagen type I expression in keloid


  • Funding sources
    This work was partly supported by 2010 CMA–L’OREAL China Skin Grant (S2010-18) and National Natural Science Foundation of China (No. 30972654, 30700717).

  • Conflicts of interest
    None declared.

  • J.L., J.C. and M.L. contributed equally to this work.

Hongxiang Chen.


Background  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.