Abstract:
OBJECTIVE:The aim of the present work was to investigate the mechanism of transforming growth factor (TGF)-β1 and Sloan-Kettering Institute (Ski) in the pathogenesis of hypertrophic scars (HS). BACKGROUND:Wound healing is an inherent process, but the aberrant wound healing of skin injury may lead to HS. There has been growing evidence suggesting a role for TGF-β1 and Ski in the pathogenesis of fibrosis. MATERIAL AND METHODS:The MTT assay was used to detect the cell proliferation induced by TGF-β1. The Ski gene was transduced into cells with an adenovirus, and then the function of Ski in cell proliferation and differentiation was observed. Ski mRNA levels were measured by RT-PCR. Western blotting was used to detect the protein expression of α-SMA, E-cadherin, Meox1, Meox2, Zeb1 and Zeb2. RESULTS:TGF-β1 can promote human skin fibroblast (HSF) cell proliferation in a time-dependent manner, but the promoting effect could be suppressed by Ski. TGF-β1 also induces the formation of the myofibroblast phenotype and the effect of TGF-β1 could be diminished by Ski. Also, Ski modulates the cardiac myofibroblast phenotype and function through suppression of Zeb2 by up-regulating the expression of Meox2. CONCLUSIONS:Ski diminishes the myofibroblast phenotype induced by TGF-β1 through the suppression of Zeb2 by up-regulating the expression of Meox2.
journal_name
Exp Mol Patholjournal_title
Experimental and molecular pathologyauthors
Chen Z,Li W,Ning Y,Liu T,Shao J,Wang Ydoi
10.1016/j.yexmp.2014.11.002subject
Has Abstractpub_date
2014-12-01 00:00:00pages
542-9issue
3eissn
0014-4800issn
1096-0945pii
S0014-4800(14)00177-4journal_volume
97pub_type
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