Collagen Triple Helix Repeat Containing 1 Inhibits TGF-?1-induced Collagen Type?Expression 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-?) 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-?, 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-?1 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-?1 invovled in the keloid pathogenesis was examined in human fibroblasts of keloids and normal skins.Methods The expression of Cthrcl and TGF-?1were investigated in fibroblasts of keloid and normal skin. The collagen type?expression and collagen synthesis in keloid fibroblasts induced by TGF-?1 were examined. Then, recombinant Cthrclwas applied to assess its correlation with TGF-?1. Results Increased TGF-?1 and Cthrcl expression were examined in keloid compared with normal skin. Cthrcl expression increased in a concentration dependent manner induced by TGF-?1 in keloid fibroblasts. TGF-?1 stimulated collagen type?expression and collagen synthesis in keloid fibroblasts which can be reversed by recombinant Cthrcl.Conclusions TGF-?1 was upregulated in keloid fibroblasts and recombinant Cthrcl inhibited TGF-?1-stimulated collagen type?synthesis which suggested Cthrcl may be a potential therapeutic option for keloids.