95 66

Cited 9 times in

Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells

DC FieldValueLanguage
dc.contributor.author이진우-
dc.date.accessioned2018-07-20T08:12:57Z-
dc.date.available2018-07-20T08:12:57Z-
dc.date.issued2017-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/160975-
dc.description.abstractTriclosan (TCS), an antimicrobial chemical with potential endocrine-disrupting properties, may pose a risk to early embryonic development and cellular homeostasis during adulthood. Here, we show that TCS induces toxicity in both the nematode C. elegans and human mesenchymal stem cells (hMSCs) by disrupting the SKN-1/Nrf2-mediated oxidative stress response. Specifically, TCS exposure affected C. elegans survival and hMSC proliferation in a dose-dependent manner. Cellular analysis showed that TCS inhibited the nuclear localization of SKN-1/Nrf2 and the expression of its target genes, which were associated with oxidative stress response. Notably, TCS-induced toxicity was significantly reduced by either antioxidant treatment or constitutive SKN-1/Nrf2 activation. As Nrf2 is strongly associated with aging and chemoresistance, these findings will provide a novel approach to the identification of therapeutic targets and disease treatment.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleTriclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Orthopedic Surgery-
dc.contributor.googleauthorDong Suk Yoon-
dc.contributor.googleauthorYoorim Choi-
dc.contributor.googleauthorDong Seok Cha-
dc.contributor.googleauthorPeng Zhang-
dc.contributor.googleauthorSeong Mi Choi-
dc.contributor.googleauthorMohammad Abdulmohsen Alfhili-
dc.contributor.googleauthorJoseph Ryan Polli-
dc.contributor.googleauthorDeQwon Pendergrass-
dc.contributor.googleauthorFaten A. Taki-
dc.contributor.googleauthorBrahmam Kapalavavi-
dc.contributor.googleauthorXiaoping Pan-
dc.contributor.googleauthorBaohong Zhang-
dc.contributor.googleauthorT. Keith Blackwell-
dc.contributor.googleauthorJin Woo Lee-
dc.contributor.googleauthorMyon-Hee Lee-
dc.identifier.doi10.1038/s41598-017-12719-3-
dc.contributor.localIdA03230-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid28974696-
dc.contributor.alternativeNameLee, Jin Woo-
dc.contributor.affiliatedAuthorLee, Jin Woo-
dc.citation.volume7-
dc.citation.number1-
dc.citation.startPage12592-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.7(1) : 12592, 2017-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Orthopedic Surgery (정형외과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.