LncRNA MIR100HG induces degenerative changes in intervertebral disc degeneration nucleus pulposus cells by targeting miR-31-5p.

BACKGROUND

To investigate the regulatory role of LncRNA MIR100HG on the functional and inflammatory levels of nucleus pulposus cells (NPCs) in intervertebral disc degeneration (IDD).

METHODS

A total of 183 patients (including 101 IDD patients) were included. Magnetic resonance imaging (MRI) assessed the degree of IDD. Intraoperative nucleus pulposus tissue was stored at - 80 °C. Logistic regression analysis identified risk factors for IDD. ROC analysis assessed the diagnostic value of LncRNA MIR100HG in predicting IDD. RT-qPCR detected gene expression, while CCK8 and flow cytometry observed cell proliferation and apoptosis. ELISA detected inflammatory factor expression. DLR and RIP validated the target relationship of genes.

RESULTS

LncRNA MIR100HG is upregulated in NP tissue from IDD patients and increases with rising Pfirrman grades. LncRNA MIR100HG is a risk factor for IDD patients and has diagnostic value in predicting IDD progression. Overexpression of LncRNA MIR100HG leads to slowed NPCs proliferation and extracellular matrix (ECM) synthesis, promoting apoptosis, increased inflammation levels, and ECM degradation. miR-31-5p is downregulated in NP tissue from IDD patients. LncRNA MIR100HG regulates NPCs function via miR-31-5p. Transfection of miR mimic can counteract the functional alterations in NPCs caused by LncRNA MIR100HG overexpression.

CONCLUSIONS

LncRNA MIR100HG targets miR-31-5p to inhibit NPCs proliferation and ECM anabolic metabolite expression, promote NPCs apoptosis and increased inflammatory levels, thereby inducing degenerative changes in NPCs.