Collagen Triple Helix Repeat Containing 1 Inhibits TGF-β1-induced Collagen TypeⅠExpression In Keloid

Background Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. There is evidence that transforming growth factor-beta (TGF-β) is involved in keloid formation. Collagen triple helix repeat containing-1 (Cthrcl) 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. To our knowledge, however, expression and regulatory mechanisms of Cthrcl and TGF-β1 in keloid and normal skin has not been studied before.Objectives Cthrcl gene regulation and potential role in keloid formation were determined. And its correlation with TGF-β1 invovled in the keloid pathogenesis was examined in human fibroblasts of keloids and normal skins.Methods The expression of Cthrcl and TGF-β1were investigated in fibroblasts of keloid and normal skin. The collagen typeⅠexpression and collagen synthesis in keloid fibroblasts induced by TGF-β1 were examined. Then, recombinant Cthrclwas applied to assess its correlation with TGF-β1. Results Increased TGF-β1 and Cthrcl expression were examined in keloid compared with normal skin. Cthrcl expression increased in a concentration dependent manner induced by TGF-β1 in keloid fibroblasts. TGF-β1 stimulated collagen typeⅠexpression and collagen synthesis in keloid fibroblasts which can be reversed by recombinant Cthrcl.Conclusions TGF-β1 was upregulated in keloid fibroblasts and recombinant Cthrcl inhibited TGF-β1-stimulated collagen typeⅠsynthesis which suggested Cthrcl may be a potential therapeutic option for keloids.