Background: Dysregulation of microRNAs (miRNAs) has been reported to be associated with Intervertebral Disc Degeneration (IDD), and accumulating evidence suggested that miR-98-5p was involved in pathogenesis of IDD, but the underlying molecular mechanisms remains elusive.
Method: MTT assay and flow cytometry were conducted to examine the viability and apoptosis of pressure-damaged cells, respectively. Computational analysis and luciferase assay were performed to identify the target of miR-98-5p. Western-blot and real-time PCR were utilized to detect miR-98-5p and BMP2 levels in the culture cells.
Results: Compression caused a time-dependent suppression of the growth of Nucleus Pulposus Cells (NPCs), and significant apoptosis was induced in the damaged cells in a time-dependent pattern compared with normal control. Bioinformatics analysis was used to validate Bone Morphogenetic Proteins 2 (BMP2) as a potential target of miR-98-5p, which was further confirmed by luciferase assay results. Experimental cells exhibited a lower level of miR-98-5p, and a higher level of BMP2. The viability of the cultured cells transfected with miR-98-5p were lower than the control, while and cells transfected with miR-98-5p antisense was found to grow faster than the negative control. The increased expression level of miR-98-5p inhibited the expression of BMP2, and knockdown miR-98-5p increased the expression of BMP2.
Conclusion: Taken together, our studies provided evidence that miR-98-5p may serve as a novel therapeutic target for IDD via modulating expression of BMP2.