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MicroRNA-338-3p as a novel therapeutic target for intervertebral disc degeneration
Hua Jiang1,2, Abu Moro3, Jiaqi Wang3
1Division of Spine Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China. drjianghua@163.com.
Abstract:
Recent studies have demonstrated the pivotal role played by microRNAs (miRNAs) in the etiopathogenesis of intervertebral disc degeneration (IDD). The study of miRNA intervention in IDD models may promote the advancement of miRNA-based therapeutic strategies. The aim of the current study was to investigate whether intradiscal delivery of miRNA can attenuate IDD development. Our results showed that miR-338-3p expression was significantly increased in the nucleus pulposus (NP) of patients with IDD. Moreover, there was a statistically significant positive correlation between the expression level of miR-338-3p and the severity of IDD. Our functional studies showed that miR-338-3p significantly influenced the expression of extracellular matrix synthesis genes, as well as the proliferation and apoptosis of NP cells. Mechanistically, miR-338-3p aggravated IDD progression by directly targeting SIRT6, a negative regulator of the MAPK/ERK pathway. Intradiscal injection of antagomir-338-3p significantly decelerated IDD development in mouse models. Our study is the first to identify miR-338-3p as a mediator of IDD and thus may be a promising target for rescuing IDD.
Insights
MicroRNAs (miRNAs) are key in intervertebral disc degeneration (IDD). This study found miR-338-3p accelerates IDD by targeting SIRT6, suggesting antagomir-338-3p as a potential therapy for IDD.
Area of Science:
- Biomedical research
- Molecular biology
- Regenerative medicine
Background:
- MicroRNAs (miRNAs) play a critical role in the development of intervertebral disc degeneration (IDD).
- Investigating miRNA intervention strategies is crucial for advancing therapeutic approaches for IDD.
Purpose of the Study:
- To investigate the role of miRNA intervention in IDD.
- To determine if intradiscal delivery of miRNA can reduce IDD progression.
Main Methods:
- Quantified miR-338-3p expression in nucleus pulposus (NP) from IDD patients.
- Assessed the correlation between miR-338-3p levels and IDD severity.
- Performed functional studies on NP cells and utilized mouse models for therapeutic intervention.
Main Results:
- miR-338-3p expression was significantly elevated in IDD patients' NP tissue.
- miR-338-3p positively correlated with IDD severity and influenced NP cell proliferation, apoptosis, and extracellular matrix gene expression.
- miR-338-3p exacerbates IDD by targeting SIRT6, a negative regulator of the MAPK/ERK pathway.
Conclusions:
- miR-338-3p is identified as a key mediator in IDD pathogenesis.
- Intradiscal administration of antagomir-338-3p effectively slowed IDD progression in mouse models.
- miR-338-3p represents a promising therapeutic target for mitigating IDD.
