Long non-coding RNA ANRIL mitigates neonatal hypoxic-ischemic brain damage via targeting the miR-378b/ATG3 axis.

Hypoxic-ischemic brain injury (HIBD) is the most common form of brain injury in newborns and is a major burden on society. However, the molecular mechanism of HIBD remains unclear. Long non-coding RNA (lncRNA) has been demonstrated to be a key regulator in brain development and numerous neurological diseases. The present study identified the role and underlying mechanism of lncRNA antisense non-coding RNA in the INK4 locus (ANRIL) in HIBD. The data indicated that ANRIL expression was significantly increased in hypoxia-stressed primary neurons and PC12 cells. Silencing ANRIL aggravated oxygen-glucose deprivation-induced cell injury. Mechanistically, microRNA (miR)-378b was predicted and confirmed as a direct target of ANRIL. A miR-378b inhibitor counteracted the effect of ANRIL on hypoxia-induced cell injury. Furthermore, ANRIL positively regulated autophagy related 3 (ATG3) expression and promoted autophagy through competitively binding to miR-378b. Overall, the present findings suggest that ANRIL exerts its protective effects via binding to miR-378b and upregulating ATG3 expression, suggesting the potential of ANRIL as a protective target for HIBD.