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Endothelial-to-mesenchymal transition induced by Wnt 3a in keloid pathogenesis.

DC Field Value Language
dc.contributor.author신정우-
dc.contributor.author양우익-
dc.contributor.author유대현-
dc.contributor.author이광훈-
dc.contributor.author이원재-
dc.contributor.author이주희-
dc.date.accessioned2016-02-04T11:44:09Z-
dc.date.available2016-02-04T11:44:09Z-
dc.date.issued2015-
dc.identifier.issn1067-1927-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/141082-
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 α-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 α-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.-
dc.description.statementOfResponsibilityopen-
dc.format.extent435~442-
dc.relation.isPartOfWOUND REPAIR AND REGENERATION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdolescent-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHCell Proliferation-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCicatrix, Hypertrophic/pathology*-
dc.subject.MESHDown-Regulation-
dc.subject.MESHEndothelial Cells/metabolism*-
dc.subject.MESHEpithelial Cells/cytology-
dc.subject.MESHEpithelial Cells/drug effects*-
dc.subject.MESHFemale-
dc.subject.MESHFibroblasts/metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHKeloid/pathology*-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHVascular Endothelial Growth Factor A-
dc.subject.MESHWnt Signaling Pathway/drug effects*-
dc.subject.MESHWnt3A Protein/pharmacology*-
dc.subject.MESHWound Healing*/drug effects-
dc.titleEndothelial-to-mesenchymal transition induced by Wnt 3a in keloid pathogenesis.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Dermatology (피부과학)-
dc.contributor.googleauthorWon Jai Lee-
dc.contributor.googleauthorJi Hun Park-
dc.contributor.googleauthorJung U. Shin-
dc.contributor.googleauthorHyun Noh-
dc.contributor.googleauthorDae Hyun Lew-
dc.contributor.googleauthorWoo Ick Yang-
dc.contributor.googleauthorChae Ok Yun-
dc.contributor.googleauthorKwang Hoon Lee-
dc.contributor.googleauthorJu Hee Lee-
dc.identifier.doi10.1111/wrr.12300-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02149-
dc.contributor.localIdA02300-
dc.contributor.localIdA02459-
dc.contributor.localIdA03005-
dc.contributor.localIdA03171-
dc.contributor.localIdA02674-
dc.relation.journalcodeJ02807-
dc.identifier.eissn1524-475X-
dc.identifier.pmid25845828-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/wrr.12300/abstract-
dc.contributor.alternativeNameShin, Jung U-
dc.contributor.alternativeNameYang, Woo Ick-
dc.contributor.alternativeNameLew, Dae Hyun-
dc.contributor.alternativeNameLee, Kwang Hoon-
dc.contributor.alternativeNameLee, Won Jai-
dc.contributor.alternativeNameLee, Ju Hee-
dc.contributor.affiliatedAuthorShin, Jung U-
dc.contributor.affiliatedAuthorYang, Woo Ick-
dc.contributor.affiliatedAuthorLew, Dae Hyun-
dc.contributor.affiliatedAuthorLee, Won Jai-
dc.contributor.affiliatedAuthorLee, Ju Hee-
dc.contributor.affiliatedAuthorLee, Kwang Hoon-
dc.rights.accessRightsnot free-
dc.citation.volume23-
dc.citation.number3-
dc.citation.startPage435-
dc.citation.endPage442-
dc.identifier.bibliographicCitationWOUND REPAIR AND REGENERATION, Vol.23(3) : 435-442, 2015-
dc.identifier.rimsid30499-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Plastic and Reconstructive Surgery (성형외과학교실) > 1. Journal Papers

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