Cited 58 times in

Advanced glycation end products (AGEs) promote melanogenesis through receptor for AGEs

DC Field Value Language
dc.contributor.author김지영-
dc.contributor.author오상호-
dc.date.accessioned2017-10-26T07:16:20Z-
dc.date.available2017-10-26T07:16:20Z-
dc.date.issued2016-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/151819-
dc.description.abstractAccumulation of advanced glycation end products (AGEs) is linked with development or aggravation of many degenerative processes or disorders, including aging and atherosclerosis. AGEs production in skin cells is known to promote stiffness and loss of elasticity through their buildup in connective tissue. However, the impact of AGEs has yet to be fully explored in melanocytes. In this study, we confirmed the existence of receptor for AGE (RAGE) in melanocytes in western blot and immunofluorescence along with increased melanin production in ex vivo skin organ culture and in vitro melanocyte culture following AGEs treatment. Cyclic AMP response element-binding protein (CREB) and extracellular signal-regulated kinases (ERK) 1/2 are considered as key regulatory proteins in AGEs-induced melanogenesis. In addition, blockage experiment using anti-RAGE blocking antibody has indicated that RAGE plays a pivotal role in AGE-mediated melanogenesis. Therefore, it is apparent that AGEs, known markers of aging, promote melanogenesis via RAGE. In addition, AGEs could be implicated in pigmentation associated with photoaging according to the results of increased secretion of AGEs from keratinocytes following UV irradiation. AGE-mediated melanogenesis may thus hold promise as a novel mean of altering skin pigmentation-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCytokines/metabolism-
dc.subject.MESHFibroblasts/cytology-
dc.subject.MESHFibroblasts/drug effects-
dc.subject.MESHFibroblasts/metabolism-
dc.subject.MESHGlycation End Products, Advanced/pharmacology*-
dc.subject.MESHHumans-
dc.subject.MESHKeratinocytes/cytology-
dc.subject.MESHKeratinocytes/drug effects-
dc.subject.MESHKeratinocytes/metabolism-
dc.subject.MESHMelanins/metabolism*-
dc.subject.MESHMelanocytes/cytology-
dc.subject.MESHMelanocytes/drug effects-
dc.subject.MESHMelanocytes/metabolism-
dc.subject.MESHMicroscopy, Confocal-
dc.subject.MESHMitogen-Activated Protein Kinase 1/metabolism-
dc.subject.MESHMitogen-Activated Protein Kinase 3/metabolism-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHReceptor for Advanced Glycation End Products/metabolism*-
dc.subject.MESHSignal Transduction/drug effects-
dc.subject.MESHSkin/metabolism-
dc.subject.MESHSkin/pathology-
dc.subject.MESHSkin Pigmentation/radiation effects-
dc.subject.MESHUltraviolet Rays-
dc.subject.MESHUp-Regulation/drug effects*-
dc.titleAdvanced glycation end products (AGEs) promote melanogenesis through receptor for AGEs-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentYonsei Biomedical Research Center-
dc.contributor.googleauthorEun Jung Lee-
dc.contributor.googleauthorJi Young Kim-
dc.contributor.googleauthorSang Ho Oh-
dc.identifier.doi10.1038/srep27848-
dc.contributor.localIdA02370-
dc.contributor.localIdA00982-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid27293210-
dc.contributor.alternativeNameKim, Ji Young-
dc.contributor.alternativeNameOh, Sang Ho-
dc.contributor.affiliatedAuthorOh, Sang Ho-
dc.contributor.affiliatedAuthorKim, Ji Young-
dc.citation.volume6-
dc.citation.startPage27848-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.6 : 27848, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid45828-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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