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Background <p>Defective apoptosis of autoreactive immune cells contributes to multiple sclerosis (MS) pathogenesis. Survivin (<i>BIRC5</i>), an anti-apoptotic protein, and interleukin-4 (<i>IL-4</i>), а cytokine with dual immunomodulatory roles, are potential key players. This study investigates the expression of <i>BIRC5</i>, <i>IL-4</i>, and three apoptosis-associated miRNAs (miR-203a, miR-3622b-5p, miR-198) in MS, focusing on their regulatory interplay.</p> Methods and results <p>Whole blood RNA from 28 relapsing-remitting MS patients and 27 healthy controls was analyzed via qRT-PCR. <i>BIRC5</i> and <i>IL-4</i> expression were significantly elevated in MS patients (<i>p</i> = 0.008; <i>p</i> = 0.012). miR-203a (<i>p</i> = 0.005) and miR-3622b-5p (<i>p</i> = 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 <i>BIRC5</i> and <i>IL-4</i>, supported by strong correlations (<i>BIRC5</i>-miR-203a: <i>r</i> = 0.65, <i>p</i> = 0.002; <i>IL-4</i>-miR-3622b-5p: <i>r</i> = 0.58, <i>p</i> = 0.007). Gene ontology analysis linked these molecules to apoptotic resistance (GO:0043066) and Th2 signaling (KEGG:04630).</p> Conclusions <p>This study reveals a dysregulated <i>BIRC5</i>/<i>IL-4</i>/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.</p>

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

  • 期刊论文

  • 发表日期：

    2025年10月9日

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

摘要

Background

Defective 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 results

Whole 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).

Conclusions

This 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.