Publication
Fingolimod Treatment Modulates PPARĪ³ and CD36 Gene Expression in Women with Multiple Sclerosis
| dc.contributor.author | Ferret-Sena, V | |
| dc.contributor.author | Capela, C | |
| dc.contributor.author | Macedo, A | |
| dc.contributor.author | Salgado, AV | |
| dc.contributor.author | Derudas, B | |
| dc.contributor.author | Staels, B | |
| dc.contributor.author | Sena, A | |
| dc.date.accessioned | 2023-02-13T12:59:03Z | |
| dc.date.available | 2023-02-13T12:59:03Z | |
| dc.date.issued | 2022-12 | |
| dc.description.abstract | Fingolimod 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 PPARĪ³ and CD36 gene expression. No correlations were found between lipid levels and variations in PPARĪ³ and CD36 gene expression. PPARĪ³ and CD36 variations were significantly correlated during therapy and in patients free of relapse and stable disease. Our results suggest that PPARĪ³ 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 PPARĪ³/CD36 pathway to the clinical efficacy of the drug and its involvement in the pathogenesis of the disease. | pt_PT |
| dc.description.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Front Mol Neurosci. 2022 Dec 15;15:1077381. doi: 10.3389/fnmol.2022.1077381 | pt_PT |
| dc.identifier.doi | 10.3389/fnmol.2022.1077381 | pt_PT |
| dc.identifier.uri | http://hdl.handle.net/10400.17/4401 | |
| dc.language.iso | eng | pt_PT |
| dc.publisher | Frontiers Media SA | pt_PT |
| dc.subject | HSAC NEU | pt_PT |
| dc.subject | Cluster of Differentiation 36 (CD36) | pt_PT |
| dc.subject | Fingolimod | pt_PT |
| dc.subject | Lipoproteins | pt_PT |
| dc.subject | Multiple Sclerosis | pt_PT |
| dc.subject | Peroxisome Proliferator-Activated Receptors (PPAR) | pt_PT |
| dc.title | Fingolimod Treatment Modulates PPARĪ³ and CD36 Gene Expression in Women with Multiple Sclerosis | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.startPage | 1077381 | pt_PT |
| oaire.citation.title | Frontiers in Molecular Neuroscience | pt_PT |
| oaire.citation.volume | 15 | pt_PT |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt_PT |