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MicroRNA-572 expression in multiple sclerosis patients with different patterns of clinical progression

BACKGROUND: Demyelination and failure of remyelination are core mechanisms in the pathogenesis of multiple sclerosis (MS); the factor(s) modulating these processes are still mostly unknown. MicroRNA 572 (miR-572) is deregulated in MS and is suggested to targets neural cell adhesion molecule (NCAM),...

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Detalles Bibliográficos
Autores principales: Mancuso, Roberta, Hernis, Ambra, Agostini, Simone, Rovaris, Marco, Caputo, Domenico, Clerici, Mario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429409/
https://www.ncbi.nlm.nih.gov/pubmed/25947625
http://dx.doi.org/10.1186/s12967-015-0504-2
Descripción
Sumario:BACKGROUND: Demyelination and failure of remyelination are core mechanisms in the pathogenesis of multiple sclerosis (MS); the factor(s) modulating these processes are still mostly unknown. MicroRNA 572 (miR-572) is deregulated in MS and is suggested to targets neural cell adhesion molecule (NCAM), a glycoprotein involved in CNS reparative mechanisms. The aim of this study is to analyze miR-572 in patients with different clinical phenotypes of MS. METHODS: qPCR quantification of miR-572 isolated from serum was performed in 16 primary progressive (PP), 15 secondary progressive (SP), 31 relapsing remitting (RR) MS patients and 15 sex-and age-matched healthy controls. RESULTS: miR-572 expression was reduced overall in MS patients (p < 0.05) compared to HC; this miRNA was significantly upregulated in SPMS and in RRMS during disease relapse, whereas it was downregulated in PPMS and in quiescent phases of RRMS. miR-572 expression correlated with EDSS scores (R(Sp) = 0.491; p < 0.05) independently of the clinical phenotype. The results suggest that this miRNA might be a tool that helps distinguishing between PPMS and SPMS and between relapsing and remitting phases in RRMS. CONCLUSIONS: Evaluation of miR-572 may serve as a non-invasive biomarker for remyelination. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12967-015-0504-2) contains supplementary material, which is available to authorized users.