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dc.creatorKolić, Ivana
dc.creatorStojković, Ljiljana S.
dc.creatorDinčić, Evica
dc.creatorJovanović, Ivan G.
dc.creatorStanković, Aleksandra
dc.creatorŽivković, Maja
dc.date.accessioned2020-05-14T12:20:19Z
dc.date.available2020-05-14T12:20:19Z
dc.date.issued2020
dc.identifier.issn0165-5728
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/8618
dc.description.abstractLeptin (LEP) may contribute to the pathogenesis of multiple sclerosis (MS) by its immunomodulatory, proinflammatory and prooxidant effects. Therefore, plasma LEP levels and mRNA expression of five genes related to the LEP signaling pathway (LEP, LEP receptor (LEPR), peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1A), superoxide dismutase 2, tumor necrosis factor-alpha) were investigated in relapsing-remitting MS. In patients (N = 64), compared to healthy subjects (N = 62), relative LEP mRNA levels were significantly increased (p = 0,01), while LEPR and PGC1A mRNA levels were decreased (p = 0,001 and p = 0,04, respectively). Significant positive correlation was observed between LEPR mRNA levels and clinical parameters of MS progression (EDSS, MSSS). © 2019en
dc.language.isoen
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175085/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41028/RS//
dc.rightsrestrictedAccess
dc.sourceJournal of Neuroimmunology
dc.subjectPeripheral blood mononuclear cellsen
dc.subjectLeptinen
dc.subjectmRNA expressionen
dc.subjectInflammationen
dc.subjectOxidative responseen
dc.subjectMultiple sclerosisen
dc.titleExpression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosisen
dc.typearticleen
dc.rights.licenseARR
dcterms.abstractЖивковић, Маја; Стојковић, Љиљана; Јовановић, Иван; Станковић, Aлександра; Колић, Ивана; Динчић, Евица;
dc.rights.holder© 2019
dc.citation.volume338
dc.citation.spage577090
dc.identifier.wos000508751300005
dc.identifier.doi10.1016/j.jneuroim.2019.577090
dc.citation.rankM22~
dc.identifier.pmid31704454
dc.type.versionpublishedVersion
dc.identifier.scopus2-s2.0-85074353466


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