Overexpression of miR-124 protects against neurological dysfunction induced by neonatal hypoxic-ischemic brain injury
Date
2020
Authors
Xiong, L.
Zhou, H.
Zhao, Q.
Xue, L.
Al Hawwas, M.
He, J.
Wu, M.
Zou, Y.
Yang, M.
Dai, J.
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Journal article
Citation
Cellular and Molecular Neurobiology, 2020; 40(5):737-750
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Abstract
Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of lifelong disabilities worldwide, without effective therapies and clear regulatory mechanisms. MicroRNAs (miRNAs) act as a significant regulator in neuroregeneration and neuronal apoptosis, thus holding great potential as therapeutic targets in HIE. In this study, we established the hypoxia-ischemia (HI) model in vivo and oxygen-glucose deprivation (OGD) model in vitro. Zea-longa score and magnetic resonance imaging were applied to verify HI-induced neuronal dysfunction and brain infarction. Subsequently, a miRNA microarray analysis was employed to profile miRNA transcriptomes. Down-regulated miR-124 was found 24 h after HIE, which corresponded to the change in PC12, SHSY5Y, and neurons after OGD. To determine the function of miR-124, mimics and lentivirus-mediated overexpression were used to regulate miR-124 in vivo and in vitro, respectively. Our results showed that miR-124 overexpression obviously promoted cell survival and suppressed neuronal apoptosis. Further, the memory and neurological function of rats was also obviously improved at 1 and 2 months after HI, indicated by the neurological severity score, Y-maze test, open field test, and rotating rod test. Our findings showed that overexpression of miR-124 can be a promising new strategy for HIE therapy in future clinical practice.
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Data source: Supplementary material, https://link.springer.com/article/10.1007%2Fs10571-019-00769-2#SupplementaryMaterial
Link to a related website: https://doi.org/10.1007/s10571-021-01178-0, Correction
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