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<p>Neonatal Encephalopathy (NE) is a clinical syndrome presenting as neurological dysfunction. Persistent dysregulated Inflammation is associated with NE and miRNA biomarkers may correlate with developmental outcomes. We investigated miR-20a, miR-20b, miR-93 and miR-532 expression at birth and childhood following Neonatal Encephalopathy (NE) as potential biomarkers of inflammation, brain development, and long-term outcomes. Blood samples were collected from neonates with NE (week 1 of life) and children post-NE (2–5 years of age) and compared to age-matched controls (Neonatal and paediatric). Whole blood was stimulated ex-vivo with lipopolysaccharide, and total RNA was extracted from serum. MiR-20a, miR-20b, miR-93 and miR-532 were identified by TaqMan<sup>®</sup> Advanced miRNA Assays. Forty-five children were recruited (<i>n</i> = 11–12 in each group). MiR-20b, miR-93 and miR-532 significantly increased in neonates with NE compared to neonatal controls. MiR-20b expression decreased in children with NE compared to neonates with NE, to childhood control levels. MiR-93 increased in control children compared to control neonatal. MiR-20b significantly decreased with lipopolysaccharide in children with NE compared to their paired neonatal NE sample. MiR-20b, miR-93, and miR-532-5p are linked to neuron development and cellular stress responses. Their dysregulated expression might indicate altered immune responses and have potential as a biomarker.</p>

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Childhood resolution of early abnormal miRNA following neonatal encephalopathy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月20日

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  • Johana M. Isaza-Correa,
  • Eman Isweisi,
  • Ronan Murphy,
  • Tim Hurley,
  • Matthew McGovern,
  • Moira O’Reilly,
  • Sean Tamgumus,
  • Graham King,
  • Mary O’Dea,
  • Lynne A Kelly,
  • Mandy Daly,
  • Jan Miletin,
  • Claudine Vavasseur,
  • John Kelleher,
  • Eva M. Jimenez-Mateos,
  • Eleanor J. Molloy

摘要

Neonatal Encephalopathy (NE) is a clinical syndrome presenting as neurological dysfunction. Persistent dysregulated Inflammation is associated with NE and miRNA biomarkers may correlate with developmental outcomes. We investigated miR-20a, miR-20b, miR-93 and miR-532 expression at birth and childhood following Neonatal Encephalopathy (NE) as potential biomarkers of inflammation, brain development, and long-term outcomes. Blood samples were collected from neonates with NE (week 1 of life) and children post-NE (2–5 years of age) and compared to age-matched controls (Neonatal and paediatric). Whole blood was stimulated ex-vivo with lipopolysaccharide, and total RNA was extracted from serum. MiR-20a, miR-20b, miR-93 and miR-532 were identified by TaqMan® Advanced miRNA Assays. Forty-five children were recruited (n = 11–12 in each group). MiR-20b, miR-93 and miR-532 significantly increased in neonates with NE compared to neonatal controls. MiR-20b expression decreased in children with NE compared to neonates with NE, to childhood control levels. MiR-93 increased in control children compared to control neonatal. MiR-20b significantly decreased with lipopolysaccharide in children with NE compared to their paired neonatal NE sample. MiR-20b, miR-93, and miR-532-5p are linked to neuron development and cellular stress responses. Their dysregulated expression might indicate altered immune responses and have potential as a biomarker.