科研之友
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摘要
P>Background Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. There is evidence that transforming growth factor (TGF)-beta 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-beta, 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-beta 1 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-beta 1 involved in keloid pathogenesis was examined in human fibroblasts of keloids and normal skin. Methods The expression of Cthrc1 and TGF-beta 1 was investigated in fibroblasts of keloid and normal skin. Collagen type I expression and collagen synthesis in keloid fibroblasts induced by TGF-beta 1 were examined. Then, recombinant Cthrc1 was applied to assess its correlation with TGF-beta 1. Results Increased TGF-beta 1 and Cthrc1 expression was examined in keloid compared with normal skin. Cthrc1 expression increased in a concentration-dependent manner induced by TGF-beta 1 in keloid fibroblasts. TGF-beta 1 stimulated collagen type I expression and collagen synthesis in keloid fibroblasts, which can be reversed by recombinant Cthrc1. Conclusions TGF-beta 1 was upregulated in keloid fibroblasts and recombinant Cthrc1 inhibited TGF-beta 1-stimulated collagen type I synthesis, which suggests that Cthrc1 may be a potential therapeutic option for keloids.
- 出版日期2011-5
- 单位山西医科大学
