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

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.