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Published on: August 10, 2018
MicroRNA-582-5p modulation of UBR5 affects inflammatory response and motor recovery after spinal cord injury
Bin Zhang1, Haidong Zhou2,3, Yue Wang4
1Department of Spinal Surgery, The 964th Hospital of PLA Joint Logistic Support Force, Changchun, China.
Purpose:
Spinal cord injury (SCI) is a serious neurological disease, and microRNA (miRNA) plays an important role in various cellular events after SCI. This study aims to explore the expression of miR-582-5p in SCI patients and its regulatory effects on apoptosis, inflammation and oxidative stress during the SCI process.
Methods:
Serum miR-582-5p was detected in 45 patients with limb fractures and 60 patients with SCI by reverse transcription-quantitative PCR (RT-qPCR). The in vitro SCI neuroinflammation model was constructed by inducing BV-2 cells with 100ng/mL lipopolysaccharide (LPS). The SCI model of mice was constructed by Allen's percussion method. The expression of miR-582-5p, apoptosis, inflammation and oxidative stress factors in in vivo and in vitro models were detected by RT-qPCR, flow cytometry, enzyme-linked immunosorbent assay (ELISA), etc. The motor function of mice in each group was evaluated by the BMS scoring method.
Results:
MiR-582-5p was significantly downregulated in SCI patients, and this result was consistent with that in both the BV-2 cell model and SCI mice model. Functionally, the upregulation of miR-582-5p improved the recovery of motor function in SCI mice and alleviated inflammatory and oxidative stress injuries. In cell experiments, it was confirmed that Ubiquitin protein ligase E3 component n-recognin 5 (UBR5) is one of the target genes of miR-582-5p, and the overexpression of UBR5 can effectively reverse the improvement effect of miR-582-5p in SCI cell models.
Conclusions:
This study reveals the key protective role of miR-582-5p in SCI and its molecular mechanism. miR-582-5p exerts the effects of reducing inflammation and oxidative stress and promoting the recovery of neurological function by targeting and inhibiting the expression of UBR5.
