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Br J Dermatol. 2011 May;164(5):1030-6.

Collagen triple helix repeat containing-1 inhibits transforming growth factor-b1-induced collagen type I expression in keloid.

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1
Department of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Abstract

BACKGROUND:

Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. There is evidence that transforming growth factor (TGF)-b 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-b, 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-b1 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-b1 involved in keloid pathogenesis was examined in human fibroblasts of keloids and normal skin.

METHODS:

The expression of Cthrc1 and TGF-b1 was investigated in fibroblasts of keloid and normal skin. Collagen type I expression and collagen synthesis in keloid fibroblasts induced by TGF-b1 were examined. Then, recombinant Cthrc1 was applied to assess its correlation with TGF-b1.

RESULTS:

Increased TGF-b1 and Cthrc1 expression was examined in keloid compared with normal skin. Cthrc1 expression increased in a concentration-dependent manner induced by TGF-b1 in keloid fibroblasts. TGF-b1 stimulated collagen type I expression and collagen synthesis in keloid fibroblasts, which can be reversed by recombinant Cthrc1.

CONCLUSIONS:

TGF-b1 was upregulated in keloid fibroblasts and recombinant Cthrc1 inhibited TGF-b1-stimulated collagen type I synthesis, which suggests that Cthrc1 may be a potential therapeutic option for keloids.

PMID:
21667528
[Indexed for MEDLINE]
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