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Preventive effects of epigallocatechin-3-O-gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts

DC FieldValueLanguage
dc.contributor.author박종철-
dc.contributor.author이미희-
dc.date.accessioned2014-12-19T17:33:14Z-
dc.date.available2014-12-19T17:33:14Z-
dc.date.issued2012-
dc.identifier.issn1942-0900-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91625-
dc.description.abstractConsidering the various pharmacological activities of epigallocatechin-3-O-gallate (EGCG) including anticancer, and anti-inflammatory, antidiabetic, and so forth, relatively less attention has been paid to the antiaging effect of EGCG on primary cells. In this study, the preventive effects of EGCG against serial passage-induced senescence were investigated in primary cells including rat vascular smooth muscle cells (RVSMCs), human dermal fibroblasts (HDFs), and human articular chondrocytes (HACs). The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs. All cells were employed with the initial passage number (PN) between 3 and 7. For inducing senescence, the cells were serially passaged at the predetermined times and intervals in the absence or presence of EGCG (50 or 100 μM). Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50 μM EGCG, while in HDFs, 100 μM EGCG could significantly prevent senescence and recover their cell cycle progression close to the normal level. Furthermore, EGCG was found to prevent serial passage- and H(2)O(2)-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected. In addition, proliferating HDFs showed similar cellular uptake of FITC-conjugated EGCG into the cytoplasm with their senescent counterparts but different nuclear translocation of it from them, which would partly account for the differential responses to EGCG in proliferating versus senescent cells. Taking these results into consideration, it is suggested that EGCG may be exploited to craft strategies for the development of an antiaging or age-delaying agent.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfOxidative Medicine and Cellular Longevity-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titlePreventive effects of epigallocatechin-3-O-gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Medical Engineering (의학공학)-
dc.contributor.googleauthorDong-Wook Han-
dc.contributor.googleauthorMi Hee Lee-
dc.contributor.googleauthorBongju Kim-
dc.contributor.googleauthorJun Jae Lee-
dc.contributor.googleauthorSuong-Hyu Hyon-
dc.contributor.googleauthorJong-Chul Park-
dc.identifier.doi10.1155/2012/850684-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00218-
dc.contributor.localIdA01662-
dc.contributor.localIdA02777-
dc.relation.journalcodeJ02455-
dc.contributor.alternativeNameKwon, Byeong Ju-
dc.contributor.alternativeNamePark, Jong Chul-
dc.contributor.alternativeNameLee, Mi Hee-
dc.contributor.affiliatedAuthorKwon, Byeong Ju-
dc.contributor.affiliatedAuthorPark, Jong Chul-
dc.contributor.affiliatedAuthorLee, Mi Hee-
dc.citation.volume2012-
dc.citation.startPage850684-
dc.citation.endPage850684-
dc.identifier.bibliographicCitationOxidative Medicine and Cellular Longevity, Vol.2012 : 850684-850684, 2012-
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Medical Engineering (의학공학교실)

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