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ArticleMolecular biology reports2025

Altered miR-203a and miR-3622b-5p expressions in multiple sclerosis: novel correlations with apoptotic gene expression profiles.

Arezoo Azarian, Samaneh Reiszadeh Jahromi, Kiana Bahramzadeh, Kolsoum Saeidi, Hoda Kamali

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 authors.

Arezoo AzarianDepartment of Biology, Faculty of Science, University of Sistan and Baluchestan, Zahedan, Iran.
Samaneh Reiszadeh JahromiDepartment of Biology, Faculty of Science, University of Sistan and Baluchestan, Zahedan, Iran. samanehreiszadeh@gmail.com.ORCID http://orcid.org/0000-0002-0108-5275
Kiana BahramzadehDepartment of Biology, Faculty of Science, University of Sistan and Baluchestan, Zahedan, Iran.
Kolsoum SaeidiDepartment of Medical Genetics, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.ORCID http://orcid.org/0000-0003-0813-3775
Hoda KamaliNeurology Research Center, Kerman University of Medical Sciences, Kerman, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDefective apoptosis of autoreactive immune cells contributes to multiple sclerosis (MS) pathogenesis. Survivin (BIRC5), an anti-apoptotic protein, and interleukin-4 (IL-4), а cytokine with dual immunomodulatory roles, are potential key players. This study investigates the expression of BIRC5, IL-4, and three apoptosis-associated miRNAs (miR-203a, miR-3622b-5p, miR-198) in MS, focusing on their regulatory interplay. METHODS AND

resultsWhole blood RNA from 28 relapsing-remitting MS patients and 27 healthy controls was analyzed via qRT-PCR. BIRC5 and IL-4 expression were significantly elevated in MS patients (p = 0.008; p = 0.012). miR-203a (p = 0.005) and miR-3622b-5p (p = 0.003) showed marked upregulation, while miR-198 remained unchanged. Bioinformatics prediction (TargetScan/ miRDB) identified conserved binding sites for miR-203a and miR-3622b-5p in the 3'UTR of BIRC5 and IL-4, supported by strong correlations (BIRC5-miR-203a: r = 0.65, p = 0.002; IL-4-miR-3622b-5p: r = 0.58, p = 0.007). Gene ontology analysis linked these molecules to apoptotic resistance (GO:0043066) and Th2 signaling (KEGG:04630).

conclusionsThis study reveals a dysregulated BIRC5/IL-4/miRNA axis in MS, where miR-203a and miR-3622b-5p potentially enhance survivin and IL-4 expression, promoting immune cell survival. These findings highlight miRNA-mediated post-transcriptional regulation as a novel therapeutic target for restoring apoptotic balance in MS.

Indexed as

ApoptosisMicroRNAsMultiple SclerosisMultiple Sclerosis, Relapsing-Remitting3' Untranslated RegionsAdultCase-Control StudiesFemaleGene Expression ProfilingGene Expression RegulationHumansInterleukin-4MaleMiddle AgedSurvivinTranscriptome3' Untranslated RegionsBIRC5 protein, humanInterleukin-4MicroRNAsMIRN203 microRNA, humanSurvivinBIRC5 (survivin)DysregulationIL-4MicroRNA (miRNA)Molecular mechanismsMultiple sclerosis

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.