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Published on: December 9, 2015
MicroRNA-29b variants and MxA expression change during interferon beta therapy in patients with relapsing-remitting
Mahtab Fattahi1, Nahid Rezaei2, Fattah Sotoudehnejad Nematalahi1
1Department of Biology, School of Basic Science, Science and Research Branch, Islamic Azad University, Poonak, Tehran, Iran.
Background:
Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system (CNS) characterized by immune-mediated demyelination and axonal injury. Myelin-reactive IFN-γ-producing Th1 cells has been shown to play an important role in the development of MS. MicroRNAs (miRNAs) are a new class of small non-coding RNA molecules about 22 nucleotides long which regulate gene expression post-transcriptionally by binding to 3' UTR of their mRNA targets, and resulting in degradation or transcriptional repression of the targeted mRNA. Accumulating evidence supports that miRNA dysregulation is linked to the pathogenesis of autoimmune diseases that include MS. miR-29b expression has been shown to be upregulated in memory CD4+T cells from relapsing-remitting MS (RR-MS) patients, which may reflect chronic Th1 inflammation. Interferon beta (IFN-β) benefits patients with MS and reduces symptoms of the RR-MS. MxA is induced by type I interferon and predicts IFN-β response in MS patients. The aim of this study was to evaluate miR-29b variants and MxA expression and serum IFN-γ level in responders and non-responders to IFN-β treatment.
Methods:
A total of 70 IFN-β treated RR-MS patients including 35 responders and 35 non-responders were enrolled. We analyzed the expression level of miR-29b variants and MxA using the peripheral blood of MS patients treated with IFN-β for more than one year. Real-time RT-PCR was performed to analyze miR-29b variants and MxA expression one year after initiation of IFN-β therapy. Serum cytokine level was measured by ELISA.
Results:
The results indicated that the expression level of miR-29b-3p changed related to IFN-β response. Moreover, miR-29b-5p was downregulated under IFN-β treatment in responders versus non-responders. MxA level was significantly decreased in the responders. There was no change in IFN-γ level following treatment with IFN-β in the MS patients.
Conclusions:
Our results might provide fundamentals for the development of new markers of the biological effects of IFN-β therapy.
Insights
This study investigated microRNA-29b (miR-29b) variants and MxA expression in multiple sclerosis (MS) patients treated with interferon beta (IFN-β). Results show miR-29b-5p downregulation in responders, suggesting potential biomarkers for IFN-β therapy effectiveness in MS.
Area of Science:
- Neuroimmunology
- Molecular Biology
- Genetics
Background:
- Multiple sclerosis (MS) is a CNS autoimmune disease involving immune-mediated demyelination.
- Myelin-reactive Th1 cells and microRNA (miRNA) dysregulation are implicated in MS pathogenesis.
- Interferon beta (IFN-β) is a treatment for relapsing-remitting MS (RR-MS), with MxA expression predicting response.
Purpose of the Study:
- To evaluate miR-29b variants and MxA expression in IFN-β responders versus non-responders with RR-MS.
- To assess serum interferon-gamma (IFN-γ) levels in relation to IFN-β treatment response.
Main Methods:
- Analysis of miR-29b variants and MxA expression in peripheral blood of 70 RR-MS patients (35 responders, 35 non-responders) after one year of IFN-β therapy.
- Real-time RT-PCR for gene expression analysis.
- ELISA for serum cytokine level measurement.
Main Results:
- miR-29b-3p expression levels showed changes related to IFN-β response.
- miR-29b-5p was significantly downregulated in IFN-β responders compared to non-responders.
- MxA levels were significantly decreased in responders; serum IFN-γ levels remained unchanged.
Conclusions:
- The findings suggest that miR-29b variants, particularly miR-29b-5p, may serve as potential biomarkers for monitoring the biological effects of IFN-β therapy in MS patients.
- Further research could establish these miRNAs as predictive markers for treatment efficacy.
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