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<p>Sudden sensorineural hearing loss (SSNHL) is an acquired idiopathic hearing loss in which recent studies have suggested that microRNAs (miRNAs) have a pathogenetic role. We assessed six specific miRNAs linked to SSNHL in serum samples drawn from 11 SSNHL patients and 11 age and sex matched controls. Quantitative real-time PCR Cycle threshold (Ct) values were normalized to an internal control to determine relative miRNA levels. Inter-group mean age, sex, mean or median normalized Ct values were compared using Independent Sample t, Chi-squared or Mann-Whitney U tests. The relative expression (ΔΔCt) of miR-210-3p, miR-23a-2p, miR18b-5p -2.75, -3.33, and − 1.29, corresponded to statistically different ΔCt values (Students T-test, <i>p</i> = 0.006; Mann-Whitney U, <i>p</i> = 0.001 and 0.02) and fold changes of 6.73, 10.87, and 2.45, respectively, in SSNHL patients compared with controls. No significant difference in the expression levels of miR-15a-5p, miR-143-3p, or miR-183-5p was found. This study supports consistent dysregulation of miR-210-3p/-23a-3p and − 18b-5p across different populations of SSNHL patients, suggesting that they play a key role in the pathogenesis of SSNHL.</p>

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Differential expression of miR-23a-3p/-210-3p and /-18b-5p in sudden sensorineural hearing loss patients: A North American cohort study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月12日

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  • Reyhaneh Abgoon,
  • Ru Guo,
  • Cole Needham,
  • Desmond A. Nunez

摘要

Sudden sensorineural hearing loss (SSNHL) is an acquired idiopathic hearing loss in which recent studies have suggested that microRNAs (miRNAs) have a pathogenetic role. We assessed six specific miRNAs linked to SSNHL in serum samples drawn from 11 SSNHL patients and 11 age and sex matched controls. Quantitative real-time PCR Cycle threshold (Ct) values were normalized to an internal control to determine relative miRNA levels. Inter-group mean age, sex, mean or median normalized Ct values were compared using Independent Sample t, Chi-squared or Mann-Whitney U tests. The relative expression (ΔΔCt) of miR-210-3p, miR-23a-2p, miR18b-5p -2.75, -3.33, and − 1.29, corresponded to statistically different ΔCt values (Students T-test, p = 0.006; Mann-Whitney U, p = 0.001 and 0.02) and fold changes of 6.73, 10.87, and 2.45, respectively, in SSNHL patients compared with controls. No significant difference in the expression levels of miR-15a-5p, miR-143-3p, or miR-183-5p was found. This study supports consistent dysregulation of miR-210-3p/-23a-3p and − 18b-5p across different populations of SSNHL patients, suggesting that they play a key role in the pathogenesis of SSNHL.