Abstract

The abnormal expression of circular RNAs (circRNAs) is associated with numerous human diseases. This study investigated the mechanism by which circRNA acts as competitive endogenous RNA in the regulation of degenerative intervertebral disc disease (IVDD). Decreased expression of circSPG21 was detected in degenerated nucleus pulposus cells (NPCs), the function of circSPG21 in NPCs was explored and verified, and the downstream target of circSPG21 was investigated. The interaction between circSPG21 and miR-1197 and its target gene (ATP1B3) was studied by online database prediction and molecular biological verification. Finally, the circSPG21/miR-1197/ATP1B3 axis was verified in the mouse tail-looping model. The expression of circSPG21 in the nucleus pulposus in IVDD was directly related to an imbalance of anabolic and catabolic factors, which affected cell senescence. circSPG21 was found to play a role in human NPCs by acting as a sponge of miR-1197 and thereby affecting ATP1B3. The regulation of circSPG21 provides a potentially effective therapeutic strategy for IVDD.

Highlights

  • Degenerative disc disease is an age-related disease[1]

  • Most cells in the degenerative group were green, indicating cell aging (Fig. 1c). Based on these results, when intervertebral disc degeneration occurs, a series of changes occur in nucleus pulposus (NP) tissue and cells

  • The factor affecting the activity of nucleus pulposus cells (NPCs) could be a new target for treating disc degeneration

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Summary

Introduction

Degenerative disc disease is an age-related disease[1]. The disc gradually loses flexibility, elasticity, and shock absorption function, and the fibrous rings that surround the disc become fragile and tear [2]. Lower back pain caused by degenerative changes in the intervertebral disc is an important reason for the decline and loss of the working ability of the population, which has severe social and economic impacts. The current clinical treatment strategy for this disease primarily focuses on alleviating symptoms and cannot prevent or treat disc degeneration[3]. An indepth understanding of the mechanism of disc degeneration has crucial scientific value and could provide a theoretical basis for identifying new prevention and treatment strategies for disc degeneration[4]

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