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dc.contributor.authorSaowanee Jeayengen_US
dc.contributor.authorAdisak Wongkajornsilpen_US
dc.contributor.authorAndrzej T. Slominskien_US
dc.contributor.authorSiwanon Jirawatnotaien_US
dc.contributor.authorSomponnat Sampattavanichen_US
dc.contributor.authorUraiwan Panichen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherUniversity of Alabama at Birminghamen_US
dc.contributor.otherBirmingham VA Medical Centeren_US
dc.date.accessioned2018-12-21T06:46:51Z
dc.date.accessioned2019-03-14T08:02:52Z-
dc.date.available2018-12-21T06:46:51Z
dc.date.available2019-03-14T08:02:52Z-
dc.date.issued2017-07-01en_US
dc.identifier.citationFree Radical Biology and Medicine. Vol.108, (2017), 918-928en_US
dc.identifier.issn18734596en_US
dc.identifier.issn08915849en_US
dc.identifier.other2-s2.0-85019551646en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85019551646&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/41862-
dc.description.abstract© 2017 The Authors Responses of melanocytes (MC) to ultraviolet (UV) irradiation can be influenced by their neighbouring keratinocytes (KC). We investigated the role of Nrf2 in regulating paracrine effects of KC on UVB-induced MC responses through phosphorylation of MAPKs in association with oxidative stress in primary human MC cocultured with primary human KC using a transwell co-culture system and small-interfering RNA-mediated silencing of Nrf2 (siNrf2). The mechanisms by which Nrf2 modulated paracrine factors including α-melanocyte-stimulating hormone (α-MSH) and paracrine effects of KC on UVB-mediated apoptosis were also assessed. Our findings showed that co-culture of MC with siNrf2-transfected KC enhanced UVB-mediated cyclobutane pyrimidine dimer (CPD) formation, apoptosis and oxidant formation, together with phosphorylation of ERK, JNK and p38 in MC. Treatment of MC with conditioned medium (CM) from Nrf2-depleted KC also increased UVB-mediated MC damage, suggesting that KC modulated UVB-mediated MC responses via paracrine effects. Additionally, depletion of Nrf2 in KC suppressed UVB-induced α-MSH levels as early as 30 min post-irradiation, although pretreatment with N-acetylcysteine (NAC) elevated its levels in CM from siNrf2-transfected KC. Furthermore, NAC reversed the effect of CM from Nrf2-depleted KC on UVB-induced apoptosis and inflammatory response in MC. Our study demonstrates for the first time that KC provided a rescue effect on UVB-mediated MC damage, although depletion of Nrf2 in KC reversed its protective effects on MC in a paracrine fashion in association with elevation of ROS levels and activation of MAPK pathways in MC. Nrf2 may indirectly regulate the paracrine effects of KC probably by affecting levels of the paracrine factor α-MSH via a ROS-dependent mechanism.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85019551646&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleNrf2 in keratinocytes modulates UVB-induced DNA damage and apoptosis in melanocytes through MAPK signalingen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1016/j.freeradbiomed.2017.05.009en_US
Appears in Collections:Scopus 2016-2017

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