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dc.contributor.author윤채옥-
dc.date.accessioned2016-11-18T04:39:26Z-
dc.date.available2016-11-18T04:39:26Z-
dc.date.issued2015-05-
dc.identifier.citationWOUND REPAIR AND REGENERATION, v. 23, NO 3, Page. 435-442en_US
dc.identifier.issn1067-1927-
dc.identifier.issn1524-475X-
dc.identifier.urihttp://onlinelibrary.wiley.com/doi/10.1111/wrr.12300/abstract-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/24465-
dc.description.abstractEndothelial-to-mesenchymal transition is a phenotypic conversion characterized by down-regulation of vascular endothelial markers and the acquisition of a mesenchymal phenotype. We hypothesized that keloid fibroblasts are of endothelial origin and that endothelial-to-mesenchymal transition substantially contributes to collagen accumulation during the development and progression of keloids. Wingless protein (Wnt-3a) protein expression was examined using immunohistochemistry in keloid tissues. Human dermal microvascular endothelial cells (HDMECs) were treated with Wnt-3a. mRNA and protein expression of endothelial (vascular endothelial cadherin) and mesenchymal (vimentin, snail family transcription factor [slug], and -smooth muscle actin) cell markers were measured using real-time RT-PCR and immunocytochemistry, respectively. Additionally, coexpression of CD31 (cluster of differentiation 31), and endothelial cell marker, and vimentin in the vascular endothelium of keloid tissues was examined using immunofluorescence. Wnt-3a overexpression was observed in human keloid tissues. Wnt-3a treatment significantly reduced vascular endothelial cadherin mRNA expression and induced vimentin and slug mRNA expression in HDMECs. HDMECs became spindle-shaped and exhibited reduced expression of CD31 and increased expression of vimentin, slug, and -smooth muscle actin. Moreover, coexpression of CD31 and vimentin was observed in the dermal vascular endothelium of keloid tissues from two patients with clinically active keloids. In conclusion, transient conversion of HDMECs to a mesenchymal phenotype may contribute to dermal fibrosis of keloid and hypertrophic scars.en_US
dc.description.sponsorshipThis work was supported by grants from the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2012-0008180, 2014051295) to WJ Lee.en_US
dc.language.isoenen_US
dc.publisherWILEY-BLACKWELLen_US
dc.subjectGROWTH-FACTOR-BETAen_US
dc.subjectHYPERTROPHIC SCARSen_US
dc.subjectIN-VIVOen_US
dc.subjectFIBROSISen_US
dc.subjectFIBROBLASTSen_US
dc.subjectMYOFIBROBLASTen_US
dc.subjectMECHANISMSen_US
dc.subjectEXPRESSIONen_US
dc.subjectCELLSen_US
dc.subjectSKINen_US
dc.titleEndothelial-to-mesenchymal transition induced by Wnt 3a in keloid pathogenesisen_US
dc.typeArticleen_US
dc.relation.no3-
dc.relation.volume23-
dc.identifier.doi10.1111/wrr.12300-
dc.relation.page435-442-
dc.relation.journalWOUND REPAIR AND REGENERATION-
dc.contributor.googleauthorLee, Won Jai-
dc.contributor.googleauthorPark, Ji Hun-
dc.contributor.googleauthorShin, Jung U.-
dc.contributor.googleauthorNoh, Hyun-
dc.contributor.googleauthorLew, Dae Hyun-
dc.contributor.googleauthorYang, Woo Ick-
dc.contributor.googleauthorYun, Chae Ok-
dc.contributor.googleauthorLee, Kwang Hoon-
dc.contributor.googleauthorLee, Ju Hee-
dc.relation.code2015000615-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF ENGINEERING[S]-
dc.sector.departmentDEPARTMENT OF BIOENGINEERING-
dc.identifier.pidchaeok-
dc.identifier.researcherIDP-3698-2015-
Appears in Collections:
COLLEGE OF ENGINEERING[S](공과대학) > BIOENGINEERING(생명공학과) > Articles
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