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

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dc.contributor.authorLi, J.
dc.contributor.authorCao, J.
dc.contributor.authorLi, M.
dc.contributor.authorYu, Y.
dc.contributor.authorYang, Y.
dc.contributor.authorXiao, X.
dc.contributor.authorWu, Z.
dc.contributor.authorWang, L.
dc.contributor.authorTu, Y.
dc.contributor.authorChen, H.
dc.date.issued2011
dc.description.abstractBackground: 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.
dc.identifier.citationBritish Journal of Dermatology, 2011; 164(5):1030-1036
dc.identifier.doi10.1111/j.1365-2133.2011.10215.x
dc.identifier.issn0007-0963
dc.identifier.urihttps://hdl.handle.net/11541.2/138192
dc.language.isoen
dc.publisherWiley-Blackwell
dc.relation.fundingCMA-L'OREAL S2010-18
dc.relation.fundingNational Natural Science Foundation of China 30972654
dc.relation.fundingNational Natural Science Foundation of China 30700717
dc.rightsCopyright 2011 The Authors
dc.source.urihttps://doi.org/10.1111/j.1365-2133.2011.10215.x
dc.subjecthidradenitis suppurativa lesions
dc.subjectprostaglandin e-2 production
dc.subjectacne inversa
dc.subjecthuman skin
dc.subjectstereology
dc.subjectultrasound
dc.subjectinfliximab
dc.subjectsebocytes
dc.subjectbacteria
dc.subjectreceptor
dc.titleCollagen triple helix repeat containing-1 inhibits transforming growth factor-β1-induced collagen type I expression in keloid
dc.typeJournal article
pubs.publication-statusPublished
ror.mmsid9916298594001831

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