Partial epithelial-mesenchymal transition in keloid scars: regulation of keloid keratinocyte gene expression by transforming growth factor-β1
作者机构：Research DepartmentShriners Hospitals for Children-CincinnatiCincinnatiOHUSA Research DepartmentShriners Hospitals for Children-CincinnatiCincinnatiOHUSA Department of SurgeryUniversity of Cincinnati College of MedicineCincinnatiOHUSA
出 版 物：《Burns & Trauma》 (烧伤与创伤（英文）)
年 卷 期：2016年第4卷第3期
页 面：199-215页
核心收录：
学科分类：1002[医学-临床医学] 100210[医学-外科学(含：普外、骨外、泌尿外、胸心外、神外、整形、烧伤、野战外)] 10[医学]
基 金：This study was supported by the Medical Research Grants(#85300 and#85500)from the Shriners Hospitals for Children.The funding agency had no role in study data collection and analysis data interpretation or writing of the manuscript
主 题：Keloid Keratinocyte Epithelial-mesenchymal transition Wound healing Scar Fibrosis
摘 要：Background:Keloids are an extreme form of abnormal scarring that result from a pathological fibroproliferative wound healing *** molecular mechanisms driving keloid pathology remain incompletely understood,hindering development of targeted,effective *** studies in our laboratory demonstrated that keloid keratinocytes exhibit adhesion abnormalities and display a transcriptional signature reminiscent of cells undergoing epithelial-mesenchymal transition(EMT),suggesting a role for EMT in keloid *** the current study,we further define the EMT-like phenotype of keloid scars and investigate regulation of EMT-related genes in ***:Primary keratinocytes from keloid scar and normal skin were cultured in the presence or absence of transforming growth factor beta 1(TGF-β1)+/-inhibitors of TGF-β1 and downstream signaling *** expression was measured using quantitative polymerase chain *** was analyzed using an in vitro wound healing *** in keloid scar and normal skin sections were localized by *** analyses utilized SigmaPlot(SyStat Software,San Jose,CA)or SAS?(SAS Institute,Cary,NC).Results:In keloid and normal keratinocytes,TGF-β1 regulated expression of EMT-related genes,including hyaluronan synthase 2,vimentin,cadherin-11,wingless-type MMTV integration site family,member 5A,frizzled 7,ADAM metallopeptidase domain 19,and *** of canonical TGF-β1 signaling in keloid keratinocytes significantly inhibited expression of these genes,and TGF-β1 stimulation of normal keratinocytes increased their *** inhibition of the extracellular signal-regulated kinase 1/2(ERK1/2)signaling pathway or the p38 mitogen-activated protein kinase pathway attenuated TGF-β1-induced expression of subsets of these *** of keloid keratinocytes,previously shown to be increased compared with normal keratinocytes,was significantly reduced by inhibition of TGF-β1 or E
维普期刊数据库