Natalizumab Treatment Modulates Peroxisome Proliferator-Activated Receptors Expression in Women with Multiple Sclerosis

Ferret-Sena, Véronique; Silva, Alexandra Maia e; Sena, Armando; Cavaleiro, Inês; Vale, José; Derudas, Bruno; Chinetti-Gbaguidi, Giulia; Staels, Bart

doi:10.1155/2016/5716415

Cited by 8 publications

(3 citation statements)

References 20 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, fingolimod therapy was not associated with alterations in serum oxLDL levels and oxLDL/LDL ratio. In line with this scenario, we have reported that the systemic inflammatory activity induced by natalizumab therapy is associated with a reduction of PPARγ and CD36 gene expressions in PMNC (Ferret-Sena et al, 2016). Dysfunctional HDL, with proinflammatory propriety, may be present in MS (Jorissen et al, 2017)and could stimulate the PPARγ/CD36 pathway (Sini et al, 2017).…”

mentioning

confidence: 60%

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

Ferret-Sena

Capela

Macedo

et al. 2022

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

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 PPARγ and CD36 gene expression. No correlations were found between lipid levels and variations in PPARγ and CD36 gene expression. PPARγ and CD36 variations were significantly correlated during therapy and in patients free of relapse and stable disease. Our results suggest that PPARγ 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 PPARγ/CD36 pathway to the clinical efficacy of the drug and its involvement in the pathogenesis of the disease.

show abstract

mentioning

confidence: 60%

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

Ferret-Sena

Capela

Macedo

et al. 2022

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In female patients, we have found an increase of PPARβ/δ mRNA and a decrease of PPARγ and CD36 mRNA expression in PBMC at three months of NTZ therapy. In contrast, PPARα was unchanged [ 197 ]. Interestingly, inflammatory activity of monocyte derived human macrophages is associated with lower PPARγ/CD36 and higher PPARβ/δ expression levels [ 198 ].…”

Section: Peroxisome Proliferator-activated Receptors (Ppar) In Msmentioning

confidence: 99%

Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis

Ferret-Sena

Capela

Sena

2018

IJMS

Self Cite

View full text Add to dashboard Cite

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system (CNS) probably caused, in most cases, by the interaction of genetic and environmental factors. This review first summarizes some clinical, epidemiological and pathological characteristics of MS. Then, the involvement of biochemical pathways is discussed in the development and repair of the CNS lesions and the immune dysfunction in the disease. Finally, the potential roles of peroxisome proliferator-activated receptors (PPAR) in MS are discussed. It is suggested that metabolic mechanisms modulated by PPAR provide a window to integrate the systemic and neurological events underlying the pathogenesis of the disease. In conclusion, the reviewed data highlight molecular avenues of understanding MS that may open new targets for improved therapies and preventive strategies for the disease.

show abstract

“…One of these mechanisms is the activation of peroxisome proliferator-activated receptors (PPARs). PPARs that were thought to have an inflammation-reducing effect have previously been studied in neuropsychiatric disorders such as schizophrenia, multiple sclerosis, and Alzheimer's [18][19][20]. PPARs are a group of nuclear receptor proteins that modulate gene expression and play a role in the modulation of transcription factors [21].…”

Section: Introductionmentioning

confidence: 99%

Serum 15-d-PGJ2 and PPARγ levels are reduced in manic episode of bipolar disorder while IL-4 levels are not affected

Erzın

Aydemir

Yüksel

et al. 2018

Psychiatry and Clinical Psychopharmacology

View full text Add to dashboard Cite

OBJECTIVES: Bipolar disorder (BD) carries a high rate of morbidity and mortality, and the clarification of its aetiology continues to be an important field of research. In recent studies, the clinical characteristics of BDs have been explained through a number of underlying factors, including cytokines, steroids, neurotrophins, mitochondrial energy generation, oxidative stress, and neurogenesis. In this study, we aimed to investigate potential associations between BDs and inflammatory processes. METHODS: Patients with mania or in remission who attended outpatient clinics of the Department of Psychiatry of the Ankara Numune Training and Research Hospital, and who were diagnosed with BD according to the DSM-V criteria, were included in the study. IBM SPSS Statistics 23 software was used for statistical analyses of the data. The normality of the distribution of continuous and discrete numerical variables was tested with a Shapiro-Wilk Test. RESULTS: In this study, the measurements and statistical analyses revealed significantly lower 15-deoxy delta12, 14-prostaglandin J2 (15d-PGJ2) and Peroxisome Proliferator-Activated Receptor-Gamma (PPARγ) levels in patients with mania in comparison to healthy controls and patients in remission. Group comparisons did not reveal any significant differences between IL-4 levels. CONCLUSIONS: This study was not a longitudinal study evaluating the same patients during both relapse and remission periods; no group of patients in a depressive episode of BD were included in the group comparisons either. Although this evidence is not adequate for a definite conclusion, the available evidence suggests that anti-inflammatory markers such as 15d-PGJ2 and IL-4 and nuclear PPARγ receptors are potential biomarkers to clarify the aetiology of BD, and these markers may be included among the therapeutic targets for future pharmacological modulations. Further studies are required in this area.

show abstract

Natalizumab Treatment Modulates Peroxisome Proliferator-Activated Receptors Expression in Women with Multiple Sclerosis

Cited by 8 publications

References 20 publications

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

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

Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis

Serum 15-d-PGJ2 and PPARγ levels are reduced in manic episode of bipolar disorder while IL-4 levels are not affected

Contact Info

Product

Resources

About