Background <p>Trigeminal neuralgia (TN) is a debilitating neuropathic pain disorder characterized by severe paroxysmal facial pain. Increasing evidence indicates that Schwann cell dysfunction and altered nerve repair mechanisms contribute to TN pathology. MicroRNAs (miRNAs), as key regulators of Schwann cell plasticity, myelination, inflammation, and nerve regeneration, represent promising biomarker candidates. This study aimed to investigate differential expression patterns of Schwann cell–associated miRNAs (miR-221-3p, miR-132-3p, miR-210-5p, miR-340-3p, miR-98-5p, miR-182-5p) in patients with trigeminal neuralgia and evaluate their diagnostic biomarker potential.</p> Methods and results <p>Expression analysis was performed using quantitative real-time PCR with 5s rRNA as the reference gene. miRNA expression levels were evaluated by qRT-PCR. Differential expression was calculated using ΔCt, ΔΔCt, and fold-change analyses. Diagnostic performance was assessed using ROC curve analysis. Integrated visualization was carried out using scatter plots, volcano plots, and z-score–normalized heatmaps. miR-221-3p was significantly upregulated in patients with trigeminal neuralgia (TN), whereas miR-340-3p and miR-182-5p were downregulated. Hierarchical clustering and principal component analysis (PCA) demonstrated a clear separation between patient and control miRNA expression profiles. In receiver operating characteristic (ROC) analyses, miR-221-3p emerged as the most powerful individual biomarker (AUC = 0.699), while the combined miRNA panel achieved high diagnostic performance (AUC = 0.89). Downregulated miRNAs reflect suppressed inhibitory signaling pathways, suggesting that miRNA profiling may provide valuable insights into Schwann cell pathology in TN.</p> Conclusions <p>The selected miRNAs, which are implicated in impaired Schwann cell repair mechanisms, represent promising molecular biomarker candidates for the diagnosis of TN and potentially for guiding therapeutic strategies.</p>

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Investigation of miRNAs affecting schwann cells in patients with trigeminal neuralgia

  • Serap Tutgun Onrat,
  • Elif Simin Issı,
  • Hasibe Nesligül Gönen,
  • Hakan Acar,
  • Ülkü Türk Börü

摘要

Background

Trigeminal neuralgia (TN) is a debilitating neuropathic pain disorder characterized by severe paroxysmal facial pain. Increasing evidence indicates that Schwann cell dysfunction and altered nerve repair mechanisms contribute to TN pathology. MicroRNAs (miRNAs), as key regulators of Schwann cell plasticity, myelination, inflammation, and nerve regeneration, represent promising biomarker candidates. This study aimed to investigate differential expression patterns of Schwann cell–associated miRNAs (miR-221-3p, miR-132-3p, miR-210-5p, miR-340-3p, miR-98-5p, miR-182-5p) in patients with trigeminal neuralgia and evaluate their diagnostic biomarker potential.

Methods and results

Expression analysis was performed using quantitative real-time PCR with 5s rRNA as the reference gene. miRNA expression levels were evaluated by qRT-PCR. Differential expression was calculated using ΔCt, ΔΔCt, and fold-change analyses. Diagnostic performance was assessed using ROC curve analysis. Integrated visualization was carried out using scatter plots, volcano plots, and z-score–normalized heatmaps. miR-221-3p was significantly upregulated in patients with trigeminal neuralgia (TN), whereas miR-340-3p and miR-182-5p were downregulated. Hierarchical clustering and principal component analysis (PCA) demonstrated a clear separation between patient and control miRNA expression profiles. In receiver operating characteristic (ROC) analyses, miR-221-3p emerged as the most powerful individual biomarker (AUC = 0.699), while the combined miRNA panel achieved high diagnostic performance (AUC = 0.89). Downregulated miRNAs reflect suppressed inhibitory signaling pathways, suggesting that miRNA profiling may provide valuable insights into Schwann cell pathology in TN.

Conclusions

The selected miRNAs, which are implicated in impaired Schwann cell repair mechanisms, represent promising molecular biomarker candidates for the diagnosis of TN and potentially for guiding therapeutic strategies.