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Background <p>Traumatic spinal cord injury (TSCI) is a traumatic disease of the central nervous system that places a heavy burden on families and society. MicroRNAs (miRNAs) are intimately related to the pathophysiological processes of TSCI. This study aimed to investigate the diagnostic performance of miR-18a-3p and its molecular mechanism in TSCI.</p> Methods <p>The 218 patients with acute spinal trauma were classified according to the ASIA criteria into a normal group (<i>n</i> = 68), an incomplete SCI (ISCI) group (<i>n</i> = 85), and a complete SCI (CSCI) group (<i>n</i> = 65). Serum samples from participants were used to evaluate the role of miR-18a-3p in clinical diagnosis. The levels of miR-18a-3p were detected by RT-qPCR. ROC curve analysis evaluated the diagnostic performance of miR-18a-3p for TSCI. PC12 cells, which was a cell line widely used in vitro neuronal models, were treated with 5&#xa0;µg/mL LPS for 12&#xa0;h to simulate an inflammatory environment. Cell viability and apoptosis were assessed via CCK-8 assays and flow cytometry. Inflammatory cytokine levels were measured by ELISA. miR-18a-3p target sites were predicted using the TargetScan database. Target relationships were validated through dual-luciferase reporter assays.</p> Results <p>Compared with the Normal group, the levels of miR-18a-3p were approximately 0.4-fold higher in ISCI patients and approximately 0.7-fold higher in CSCI patients. ROC curve analysis revealed that miR-18a-3p had good diagnostic value for TSCI. It also distinguished between ISCI and CSCI patients. Additionally, the content of miR-18a-3p in patient serum had positive correlations with inflammatory cytokines (TNF-α, IL-1β, and IL-6). DLST was a target site of miR-18a-3p. In cell models, transfection with miR-18a-3p inhibitor enhanced cell viability and the levels of SOD and GSH. Meanwhile it suppressed proliferation, inflammatory factors and MDA levels. si-DLST attenuated the effects of the miR-18a-3p inhibitor.</p> Conclusion <p>miR-18a-3p may be a potential diagnostic marker for TSCI. Mechanistically, downregulated miR-18a-3p inhibits apoptosis, inflammation and oxidative stress by negatively modulating DLST, thereby mitigating the progression of TSCI.</p>

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The clinical significance of miR-18a-3p in traumatic spinal cord injury and its functional role in mediating apoptosis, inflammation and oxidative stress

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Yingnan Li,
  • Bin Dai,
  • Zhijian Cheng,
  • Meini Cen

摘要

Background

Traumatic spinal cord injury (TSCI) is a traumatic disease of the central nervous system that places a heavy burden on families and society. MicroRNAs (miRNAs) are intimately related to the pathophysiological processes of TSCI. This study aimed to investigate the diagnostic performance of miR-18a-3p and its molecular mechanism in TSCI.

Methods

The 218 patients with acute spinal trauma were classified according to the ASIA criteria into a normal group (n = 68), an incomplete SCI (ISCI) group (n = 85), and a complete SCI (CSCI) group (n = 65). Serum samples from participants were used to evaluate the role of miR-18a-3p in clinical diagnosis. The levels of miR-18a-3p were detected by RT-qPCR. ROC curve analysis evaluated the diagnostic performance of miR-18a-3p for TSCI. PC12 cells, which was a cell line widely used in vitro neuronal models, were treated with 5 µg/mL LPS for 12 h to simulate an inflammatory environment. Cell viability and apoptosis were assessed via CCK-8 assays and flow cytometry. Inflammatory cytokine levels were measured by ELISA. miR-18a-3p target sites were predicted using the TargetScan database. Target relationships were validated through dual-luciferase reporter assays.

Results

Compared with the Normal group, the levels of miR-18a-3p were approximately 0.4-fold higher in ISCI patients and approximately 0.7-fold higher in CSCI patients. ROC curve analysis revealed that miR-18a-3p had good diagnostic value for TSCI. It also distinguished between ISCI and CSCI patients. Additionally, the content of miR-18a-3p in patient serum had positive correlations with inflammatory cytokines (TNF-α, IL-1β, and IL-6). DLST was a target site of miR-18a-3p. In cell models, transfection with miR-18a-3p inhibitor enhanced cell viability and the levels of SOD and GSH. Meanwhile it suppressed proliferation, inflammatory factors and MDA levels. si-DLST attenuated the effects of the miR-18a-3p inhibitor.

Conclusion

miR-18a-3p may be a potential diagnostic marker for TSCI. Mechanistically, downregulated miR-18a-3p inhibits apoptosis, inflammation and oxidative stress by negatively modulating DLST, thereby mitigating the progression of TSCI.