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Fingolimod treatment modulates PPARĪ³ and CD36 gene expression in women with multiple sclerosis

2022-12Journal article Open access
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dc.contributor.authorFerret-Sena, VĆ©ronique
dc.contributor.authorCapela, Carlos
dc.contributor.authorMacedo, Ana
dc.contributor.authorSalgado, AntĆ³nio Vasco
dc.contributor.authorDerudas, Bruno
dc.contributor.authorStaels, Bart
dc.contributor.authorSena, Armando
dc.date.accessioned2023-02-13T10:15:57Z
dc.date.available2023-02-13T10:15:57Z
dc.date.issued2022-12
dc.description.abstractFingolimod is an oral immunomodulatory drug used in the treatment of multiple sclerosis (MS) that may change lipid metabolism. Peroxisome proliferator-activated receptors (PPAR) are transcription factors that regulate lipoprotein metabolism and immune functions and have been implicated in the pathophysiology of MS. CD36 is a scavenger receptor whose transcription is PPAR regulated. The objective of this study was to evaluate whether fingolimod treatment modifies PPAR and CD36 gene expression as part of its action mechanisms. Serum lipoprotein profiles and PPAR and CD36 gene expression levels in peripheral leukocytes were analysed in 17 female MS patients before and at 6 and 12 months after fingolimod treatment initiation. Clinical data during the follow-up period of treatment were obtained. We found that fingolimod treatment increased HDL-Cholesterol and Apolipoprotein E levels and leukocyte PPAR gamma and CD36 gene expression. No correlations were found between lipid levels and variations in PPAR gamma and CD36 gene expression. PPAR gamma and CD36 variations were significantly correlated during therapy and in patients free of relapse and stable disease. Our results suggest that PPAR gamma and CD36-mediated processes may contribute to the mechanisms of action of fingolimod in MS. Further studies are required to explore the relation of the PPAR gamma/CD36 pathway to the clinical efficacy of the drug and its involvement in the pathogenesis of the disease.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.3389/fnmol.2022.1077381pt_PT
dc.identifier.issn1662-5099
dc.identifier.urihttp://hdl.handle.net/10400.1/19063
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontiers Mediapt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectFingolimodpt_PT
dc.subjectPeroxisome proliferator-activated receptors (PPAR)pt_PT
dc.subjectCluster of differentiation 36 (CD36)pt_PT
dc.subjectLipoproteinspt_PT
dc.subjectMultiple sclerosispt_PT
dc.titleFingolimod treatment modulates PPARĪ³ and CD36 gene expression in women with multiple sclerosispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.titleFrontiers in Molecular Neurosciencept_PT
oaire.citation.volume15pt_PT
person.familyNameMacedo
person.givenNameAna
person.identifier.ciencia-id8414-F029-8182
person.identifier.orcid0000-0002-6978-8989
person.identifier.ridL-9912-2018
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication8e798bcb-5052-47b0-a050-32f40328cc1a
relation.isAuthorOfPublication.latestForDiscovery8e798bcb-5052-47b0-a050-32f40328cc1a

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