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<p>MicroRNAs (miRNAs) have emerged as critical epigenetic regulators in the pathogenesis of childhood bronchial asthma. This study employed high-throughput sequencing to explore miRNA expression profiles in an asthma cohort, with a focus on elucidating the functional mechanisms of key miRNAs. Notably, among the miRNAs validated by RT-qPCR, miR-31-5p exhibited the largest area under the curve (AUC) value and demonstrated significant anti-inflammatory effects in an OVA-induced allergic inflammation mouse model. Bioinformatics analysis and dual-luciferase reporter assays confirmed that TBXA2R is a direct target of miR-31-5p. Mechanistically, stimulation with house dust mite (HDM) and IL-4 downregulated miR-31-5p expression in A549 cells, accompanied by elevated levels of TBXA2R and eotaxins (CCL11, CCL24, CCL26). Conversely, overexpression of miR-31-5p suppressed TBXA2R-mediated eotaxin production. These findings highlight the significant role of miR-31-5p in peripheral blood mononuclear cells (PBMCs) of asthmatic children, suggesting its potential involvement in upregulating eotaxin expression in A549 cells through negative regulation of TBXA2R.</p>

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MicroRNA expression in peripheral blood of children with asthma and the role of miR-31-5p in childhood asthma progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月31日

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  • Wenwei Luo,
  • Gang Li,
  • Luting Zhou,
  • Ting Wang,
  • Jiawei Chen,
  • Heting Dong,
  • Li Huang,
  • Canhong Zhu,
  • Yongdong Yan,
  • Liwen Zhang,
  • Yu Wan,
  • Zhengrong Chen

摘要

MicroRNAs (miRNAs) have emerged as critical epigenetic regulators in the pathogenesis of childhood bronchial asthma. This study employed high-throughput sequencing to explore miRNA expression profiles in an asthma cohort, with a focus on elucidating the functional mechanisms of key miRNAs. Notably, among the miRNAs validated by RT-qPCR, miR-31-5p exhibited the largest area under the curve (AUC) value and demonstrated significant anti-inflammatory effects in an OVA-induced allergic inflammation mouse model. Bioinformatics analysis and dual-luciferase reporter assays confirmed that TBXA2R is a direct target of miR-31-5p. Mechanistically, stimulation with house dust mite (HDM) and IL-4 downregulated miR-31-5p expression in A549 cells, accompanied by elevated levels of TBXA2R and eotaxins (CCL11, CCL24, CCL26). Conversely, overexpression of miR-31-5p suppressed TBXA2R-mediated eotaxin production. These findings highlight the significant role of miR-31-5p in peripheral blood mononuclear cells (PBMCs) of asthmatic children, suggesting its potential involvement in upregulating eotaxin expression in A549 cells through negative regulation of TBXA2R.