ArticleInternational journal of experimental pathology2023
Abnormal expression and role of MicroRNA-214-3p/SLC8A1 in neonatal Hypoxic-Ischaemic encephalopathy.
Article in International journal of experimental pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Childhood resolution of early abnormal miRNA following neonatal encephalopathy.Scientific reports · 2025Observational
- Identification and study of mood-related biomarkers and potential molecular mechanisms in type 2 diabetes mellitus.Journal of molecular histology · 2025Article
- SLC8A1, a novel prognostic biomarker and immunotherapy target in RSA and UCEC based on scRNA-seq and pan-cancer analysis.Heliyon · 2024Article
- Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide-induced endothelial cell injury.International journal of experimental pathology · 2023Article
- Abnormal expression and role of MicroRNA-214-3p/SLC8A1 in neonatal Hypoxic-Ischaemic encephalopathy.International journal of experimental pathology · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Neonatal hypoxic-ischaemic encephalopathy (HIE) refers to brain damage caused by intra-uterine distress and asphyxia/hypoxia during the perinatal and neonatal periods. MicroRNA (MiR)-214-3p plays a critical role in cell growth and apoptosis. The aim of this study was to investigate the expression and role of miR-214-3p in neonatal HIE development, and to explore the underlying mechanisms. The expression of miR-214-3p was significantly down-regulated, while that of Slc8a1, a direct target of miR-214-3p, was significantly up-regulated, in the brain tissue of neonatal HIE rats. The over-expression of miR-214-3p promoted the proliferation and inhibited the apoptosis of neurones, while its down-regulation had the opposite effect. Our results indicate that miR-214-3p expression was down-regulated in neonatal HIE rats, and the up-regulation of miR-214-3p expression protected against HIE development by inhibiting neuronal apoptosis.
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