MicroRNA‐410 serves as a candidate biomarker in hypoxic‐ischemic encephalopathy newborns and provides neuroprotection in oxygen‐glucose deprivation‐injured PC12 and SH‐SY5Y cells

Abstract Background MicroRNA‐410 (miR‐410) has been found to be deregulated in neonatal hypoxic‐ischemic encephalopathy (HIE). However, the clinical significance and biological function of miR‐410 remain largely elusive. This study aims to investigate the expression and diagnostic performance of miR‐410 in HIE newborns, and explores the neuroprotective effect of miR‐410 in an oxygen‐glucose deprivation (OGD)‐induced cell injury model. Methods Expression of miR‐410 was examined using quantitative real‐time PCR, and its diagnostic performance was evaluated using a receiver operating characteristic analysis. We used OGD‐injured PC12 and SH‐SY5Y cells to construct an in vitro HIE model. The effect of miR‐410 on OGD‐induced cell injury was analyzed by assessing cell viability and apoptosis. Enzyme‐linked immunosorbent assay was used to evaluate inflammation in cell model. A target gene was assessed according to the luciferase reporter assay. Results Serum miR‐410 expression was significantly decreased in HIE newborns and OGD‐injured cell model. The reduced miR‐410 expression served as a biomarker for the diagnosis and progression of HIE. The OGD‐induced impaired cell viability, enhanced cell apoptosis, and activated neuroinflammation were abrogated by the overexpression of miR‐140 in both PC12 and SH‐SY5S cells. Regarding the mechanisms underlying the function of miR‐410, phosphatase and tensin homolog (PTEN) was proposed as a direct target of miR‐410. Conclusion All data revealed that serum downregulated miR‐410 in HIE serves as candidate diagnostic biomarker, and that miR‐410 exerts a neuroprotective role in OGD‐injured cells by improving cell viability and inhibiting cell apoptosis through targeting PTEN.