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Heat Shock Protein 90 Inhibitor (17-AAG) Induces Apoptosis and Decreases Cell Migration/Motility of Keloid Fibroblasts

DC FieldValueLanguage
dc.contributor.author박종철-
dc.contributor.author유대현-
dc.contributor.author윤인식-
dc.contributor.author이미희-
dc.contributor.author이원재-
dc.contributor.author나동균-
dc.date.accessioned2016-02-04T11:28:08Z-
dc.date.available2016-02-04T11:28:08Z-
dc.date.issued2015-
dc.identifier.issn0032-1052-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/140490-
dc.description.abstractBACKGROUND: The regulation of apoptosis, proliferation, and migration of fibroblasts is altered in keloids. The 90-kDa heat shock protein (heat shock protein 90) is known to play a key role in such regulation. Therefore, the authors investigated whether the inhibition of heat shock protein 90 in keloid fibroblasts could induce apoptosis and attenuate keloid fibroblast proliferation and migration. METHODS: The authors evaluated heat shock protein 90 expression in keloid tissues with immunohistochemistry. The authors used cell viability [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assays and annexin V/propidium iodide staining for apoptosis, a wound healing model and cell tracking system to assess cell migration, and Akt Western blotting analysis in keloid fibroblasts after inhibition of heat shock protein 90 with 17-allylaminodemethoxygeldanamycin (17-AAG). RESULTS: The expression of heat shock protein 90 in keloid tissues was significantly increased compared with normal tissues. The 17-AAG-treated keloid fibroblasts showed significantly decreased proliferation, promotion of apoptosis, and decreased expression of Akt. Furthermore, a dose-dependent decrease in cell migration was noted after 17-AAG treatment of keloid fibroblasts. The 17-AAG-treated keloid fibroblasts had less directionality to the wound center and migrated a shorter distance. CONCLUSIONS: The authors confirmed that the inhibition of heat shock protein 90 in keloid fibroblasts could promote apoptosis and attenuate proliferation and migration of keloid fibroblasts. Therefore, the authors think that the inhibition of heat shock protein 90 is a key factor in the regulation of biological processes in keloids. With further preclinical study, the authors will be able to apply these results clinically for keloid treatment.-
dc.description.statementOfResponsibilityopen-
dc.format.extent44e~53e-
dc.relation.isPartOfPLASTIC AND RECONSTRUCTIVE SURGERY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/drug effects*-
dc.subject.MESHBenzoquinones/pharmacology*-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHCell Line-
dc.subject.MESHCell Movement/drug effects*-
dc.subject.MESHCell Proliferation/drug effects-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHFibroblasts/drug effects*-
dc.subject.MESHFibroblasts/metabolism-
dc.subject.MESHHSP90 Heat-Shock Proteins/antagonists & inhibitors-
dc.subject.MESHHSP90 Heat-Shock Proteins/metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHIn Vitro Techniques-
dc.subject.MESHKeloid/metabolism*-
dc.subject.MESHKeloid/pathology-
dc.subject.MESHKeloid/physiopathology-
dc.subject.MESHLactams, Macrocyclic/pharmacology*-
dc.titleHeat Shock Protein 90 Inhibitor (17-AAG) Induces Apoptosis and Decreases Cell Migration/Motility of Keloid Fibroblasts-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Medical Engineering (의학공학)-
dc.contributor.googleauthorYun, In Sik-
dc.contributor.googleauthorLee, Mi Hee-
dc.contributor.googleauthorRah, Dong Kyun-
dc.contributor.googleauthorLew, Dae Hyun-
dc.contributor.googleauthorPark, Jong-Chul-
dc.contributor.googleauthorLee, Won Jai-
dc.identifier.doi10.1097/PRS.0000000000001362-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01662-
dc.contributor.localIdA02459-
dc.contributor.localIdA02588-
dc.contributor.localIdA03005-
dc.contributor.localIdA01229-
dc.contributor.localIdA02777-
dc.relation.journalcodeJ02534-
dc.identifier.eissn1529-4242-
dc.identifier.pmid26111331-
dc.identifier.urlhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00006534-201507000-00014&LSLINK=80&D=ovft-
dc.contributor.alternativeNamePark, Jong Chul-
dc.contributor.alternativeNameLew, Dae Hyun-
dc.contributor.alternativeNameYun, In Sik-
dc.contributor.alternativeNameLee, Mi Hee-
dc.contributor.alternativeNameLee, Won Jai-
dc.contributor.alternativeNameRah, Dong Kyun-
dc.contributor.affiliatedAuthorPark, Jong Chul-
dc.contributor.affiliatedAuthorLew, Dae Hyun-
dc.contributor.affiliatedAuthorYun, In Sik-
dc.contributor.affiliatedAuthorLee, Won Jai-
dc.contributor.affiliatedAuthorRah, Dong Kyun-
dc.contributor.affiliatedAuthorLee, Mi Hee-
dc.rights.accessRightsnot free-
dc.citation.volume136-
dc.citation.number1-
dc.citation.startPage44-
dc.citation.endPage53-
dc.identifier.bibliographicCitationPLASTIC AND RECONSTRUCTIVE SURGERY, Vol.136(1) : 44-53, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Medical Engineering (의학공학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Plastic and Reconstructive Surgery (성형외과학교실) > 1. Journal Papers

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