The expression profile of HAR1A and HAR1B in the peripheral blood cells of multiple sclerosis patients.
Mol Biol Rep
; 50(3): 2391-2398, 2023 Mar.
Article
em En
| MEDLINE
| ID: mdl-36583781
BACKGROUND: Multiple sclerosis (MS) is a progressive neurodegenerative disease of the central nervous system (CNS) with varying degrees of axonal and neuronal damage. The onset and progression of the disease are influenced by several environmental and genetic variables. Long non-coding RNAs (lncRNAs) have a crucial role in the pathophysiology of MS. Our study aimed to assess the levels of HAR1A and HAR1B lncRNA expression in the blood samples of MS patients and investigate the relationship between these lncRNAs and disease activity. METHODS AND RESULTS: The blood samples of 100 MS patients, including 82 relapsing-remitting (RR), 8 primary progressive (PP), and 10 secondary progressive (SP) MS cases, and 100 healthy controls were collected. Quantitative real-time PCR was used for the evaluation of gene expression. ROC curve analysis was performed to evaluate the diagnostic potential of lncRNA levels. A significant decrease was detected in HAR1A expressions (P < 0.0001), and a moderate increase was also shown in HAR1B of SPMS patients (P value = 0.0189). HAR1A showed different expression levels in patients over forty (P value = 0.034). The expression levels of HAR1A and HAR1B were positively correlated in MS patients (r = 0.2003, P value = 0.0457). In addition, ROC curve results suggested that HAR1A can be introduced as a novel biomarker for MS diagnosis (AUC = 0.776). CONCLUSION: The low serum level of HAR1A may be a potential molecular biomarker for MS diagnosis; however, no discernible difference was detected in the expression level of HAR1B in the blood samples of MS patients.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doenças Neurodegenerativas
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RNA Longo não Codificante
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Esclerose Múltipla
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article