• Li Li, Lei Zhang, and Yan Zhang.
• Nursing Department, Luoyang Central Hospital affiliated to Zhengzhou University, Zhengzhou, Henan, P.R. China.
• World Neurosurg. 2018 Dec 30.

ObjectiveIn this study, we focused on the regulatory roles of miR-494 in the pathogenesis of intervertebral disk degeneration (IDD) and the related mechanism.MethodsFirst, rat IDD models were established, and the expression levels of miR-494 in IDDs of the rats were examined. Next, human nucleus pulposus (NP) cells were cultured and transfected with miR-494 mimics and inhibitors, and the roles of miR-494 on the proliferation and apoptosis of cells were determined using MTT cell proliferation assay and flow cytometry methods. Furthermore, the targeting relationship between miR-494 and neuro-oncological ventral antigen 1 (NOVA1) was examined by dual luciferase reporter assay. Finally, the expression of NOVA1, Caspase-3, Bcl-2-associated X protein (BAX), and B-cell lymphoma-2 (BCL-2) was examined using real-time quantitative polymerase chain reaction and western blot methods.ResultsThe results demonstrated that the expression of miR-494 was significantly upregulated in IDD rats. Moreover, transfection of miR-494 inhibitors induced a significant increase in the proliferation and marked decrease in the apoptosis of the degenerated human NP cells. Transfection of miR-494 mimics has shown the opposite effects. Furthermore, NOVA1 has been confirmed as a target of miR-494, and the expressions of NOVA1 were significantly downregulated in IDD rats. In addition, transfection of miR-494 inhibitors significantly decreased the expression of Caspase-3 and BAX and markedly increased the expression of NOVA1 and BCL-2. Transfection of miR-494 mimics has shown the opposite effects.ConclusionsmiR-494 was upregulated in IDD, and miR-494 might regulate the proliferation and apoptosis of NP cells through targeting NOVA1.Copyright © 2018 Elsevier Inc. All rights reserved.

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