LncRNA OIP5-AS1 targets miR-25-3p to accelerate intervertebral disc degeneration

Abstract

Background Long noncoding RNAs (lncRNAs) have been validated to exert vital roles in intervertebral disc degeneration (IDD). However, the effect of OIP5-AS1 on IDD is unknown. This research intends to explore the function of OIP5-AS1 in IDD. Methods RT-PCR was utilized to detect levels of OIP5-AS1, miR-25-3p, Collagen II and Aggrecan in IDD tissues and NPCs. Immunofluorescence assay measured Collagen II expression. CCK-8, EdU, and flow cytometry estimated the levels of proliferation and apoptosis. Collagen II and Aggrecan proteins were assessed via western blot. The binding affinity of OIP5-AS1 with miR-25-3p was investigated by luciferase reporter assay. Enzyme-linked immunosorbent assay (ELISA) dissected the levels of inflammatory factors such as IL-6, TNF-α, IL-10 and IL-1β. Results OIP5-AS1 was high expressed in IDD tissues and its expression gradually promoted with the increasing of Pfirrmann scores. The cell morphology of NPCs changed into spindle-shaped, and Collagen II expression was low. After OIP5-AS1 was silenced, cell proliferation was boosted whereas both apoptosis and extracellular matrix (ECM) degradation were restrained. In LPS-activated NPCs, OIP5-AS1 depletion also suppressed inflammation response. Further, miR-25-3p was a target of OIP5-AS1. The effects of OIP5-AS1 silence on proliferation, apoptosis and ECM degradation were reversed upon miR-25-3p downregulation. Moreover, the inhibitory impact of OIP5-AS1 knockdown on the inflammation of LPS-treated NPCs was rescued with miR-25-3p inference. Conclusion Totally, lncRNA OIP5-AS1 targeting miR-25-3p exerted promoting effects in IDD due to its high expression, implying the usage of OIP5-AS1/miR-25-3p as a novel regulatory axis for the molecular targets of IDD therapy.