Journal
CELL CYCLE
Volume 19, Issue 1, Pages 24-38Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2019.1691763
Keywords
MicroRNA-23a-3p; traumatic brain injury; primary cortical neurons
Categories
Funding
- National Natural Science Foundation of China [81501897]
- Shanghai Municipal Commission of Health and Family Planning of Science and Research Fund [20154Y0070]
- Hong Kong K.C. Wong Educational Foundation
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Secondary brain damage plays an important role in Traumatic brain injury (TBI) and inhibition of this damage has benefit for TBI treatment. However, the pathogenesis of secondary brain damage remains largely unknown. Here, we tried to explore the influence of microRNAs (miRNAs) on neuron apoptosis and inflammatory response after TBI. Firstly, the miRNA expression profiles were analyzed in the cerebral cortex tissues from the TBI mice model (controlled cortical impact) using miRNA microarray. miR-23a-3p (miR-23a) attracted our attention as its suppressive effects on apoptosis and inflammation. The further results showed that miR-23a upregulation improved long-term neurological function, the neuron apoptosis, and inhibited neuroinflammation, whereas knockdown of miR-23a had an opposite result. Using etoposide-induced primary cortical neurons injury model, we found that miR-23a was decreased in this cell model and miR-23a overexpression-suppressed etoposide induced the activity of caspase 3 and the releases of inflammatory mediators in primary cortical neurons. Phosphatase and tensin homolog (PTEN), a well-known regulator of the AKT/mTOR pathway, was found to be a direct target of miR-23a in the primary cortical neurons. Most importantly, it was found that miR-23a overexpression reactivated the AKT/mTOR pathway in TBI mice model, as demonstrated by the upregulation of phosphorylated (p-)AKT and p-mTOR. Taken together, these data indicate that miR-23a may serve as a therapeutic target for the treatment of TBI.
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