Melatonin reverses the oxidative stress and mitochondrial dysfunction caused by LETM1 silencing

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dc.authorid0000-0001-5291-8620
dc.authorid0000-0002-1224-442X
dc.authorid0000-0002-6044-1372
dc.authorscopusid6602491471
dc.authorscopusid57212309470
dc.authorscopusid8416126500
dc.authorscopusid56769801000
dc.authorwosidsirin, duygu yasar/AAR-8685-2020
dc.authorwosidBircan, Rifat/A-7344-2018
dc.contributor.authorAral, Cenk
dc.contributor.authorDemirkesen, Seyma
dc.contributor.authorBircan, Rifat
dc.contributor.authorYasar Şirin, Duygu
dc.date.accessioned2022-05-11T14:28:41Z
dc.date.available2022-05-11T14:28:41Z
dc.date.issued2020
dc.departmentFakülteler, Fen Edebiyat Fakültesi, Biyoloji Bölümü
dc.description.abstractLETM1 is a mitochondrial inner-membrane protein, which is encoded by a gene present in a locus of 4p, which, in turn, is deleted in the Wolf-Hirschhorn Syndrome, and is assumed to be related to its pathogenesis. The cellular damage caused by the deletion is presumably related to oxidative stress. Melatonin has many beneficial roles in protecting mitochondria by scavenging reactive oxygen species, maintaining membrane potential, and improving functions. The aim of this study was to investigate the effects of melatonin administration to LETM1-silenced mouse embryonic fibroblast cells as a cellular model for LETM1 deficiency. We transfected mouse embryonic fibroblast cells with a pair of siRNA against LETM1 and monitored the oxidative stress and mitochondrial functions with or without melatonin addition. MnSOD expression and aconitase activity decreased and oxidized protein levels increased in LETM1-silenced cells. LETM1 suppression did not alter the expression of OXPHOS complexes, but the oxygen consumption rates decreased significantly; however, this change was not related to complex I but instead involved complex IV and complex II. Melatonin supplementation effectively normalized the parameters studied, including the oxygen consumption rate. Our findings identified a novel effect of LETM1 deficiency on cellular respiration via complex II as well as a potential beneficial role of melatonin treatment. On the other hand, these effects may be specific to the cell line used and need to be verified in other cell lines.
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [115S455]
dc.description.sponsorshipThis study was supported by a grant (Grant no: 115S455) from The Scientific and Technological Research Council of Turkey (TUBITAK).
dc.identifier.doi10.1002/cbin.11274
dc.identifier.endpage807
dc.identifier.issn1065-6995
dc.identifier.issn1095-8355
dc.identifier.issue3en_US
dc.identifier.pmid31777134
dc.identifier.scopus2-s2.0-85076424811
dc.identifier.scopusqualityQ1
dc.identifier.startpage795
dc.identifier.urihttps://doi.org/10.1002/cbin.11274
dc.identifier.urihttps://hdl.handle.net/20.500.11776/6911
dc.identifier.volume44
dc.identifier.wosWOS:000502154400001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAral, Cenk
dc.institutionauthorDemirkesen, Seyma
dc.institutionauthorBircan, Rifat
dc.institutionauthorYasar Şirin, Duygu
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofCell Biology International
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectLETM1
dc.subjectmelatonin
dc.subjectMnSOD
dc.subjectoxidative phosphorylation complexes
dc.subjectoxidative stress
dc.subjectWolf-Hirschhorn Syndrome
dc.subjectWolf-Hirschhorn-Syndrome
dc.subjectRat-Brain
dc.subjectMetabolism
dc.subjectDefects
dc.subjectDamage
dc.subjectHomeostasis
dc.subjectExpression
dc.subjectIncreases
dc.subjectInteracts
dc.subjectProtects
dc.titleMelatonin reverses the oxidative stress and mitochondrial dysfunction caused by LETM1 silencing
dc.typeArticle

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