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MiR-23b was frequently downregulated in TBI patients and experimental TBI model.Overexpression of miR-23b attenuated brain injury in rat model of TBI.Overexpression of miR-23b improved TBI-induced neurological and cognitive impairmentss.Overexpression of miR-23b inhibited TBI-induced the activation of neuronal autophagy in the rat hippocampus CA1 region.Autophagy-related gene, ATG12, was a novel target of miR-23b.miR-23b improved TBI-induced cognitive impairments by directly targeting ATG12 to suppress neuronal autophagy.Dysregulated microRNAs (miRNAs) have been reported to involve in the pathophysiological process of traumatic brain injury (TBI), and modulate autophagy-related genes (ATGs) expression. Our previous studies showed that neuronal autophagy was activated in the injury hippocampus post- TBI and associated with neurological and cognitive impairments. The present study was designed to investigate the possible role of miR-23b in TBI-induced cognitive impairments. We found the overexpression of miR-23b conferred a better neuronprotective effects after TBI by decreasing lesion volume, alleviating brain edema, inhibiting neuron apoptosis and attenuating long-term neurological deficits, and most interestingly, improving cognitive impairments. To further explore the molecular underlying this neuronprotection, we evaluated autophagic activity and ATG12 expression in the injury hippocampus CA1 region. The results identified that miR-23b directly targeted to the 3′UTR region of ATG12 mRNA to suppress the activation of neuronal autophagy by a dual-luciferase reporter system. Notably, overexpression of ATG12 abrogated the neuronprotective effects of miR-23b on TBI-induced neurological and cognitive impairments. Taken together, these date revealed inhibition of ATG12-mediated autophagic activity by miR-23b overexpression might be involve in cognitive improvement after TBI, indicating that miR-23b might be a potential therapeutic target for TBI.