Childhood resolution of early abnormal miRNA following neonatal encephalopathy

Abstract

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.