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Background <p>Spinal cord injury (SCI) remains a devastating neurological condition for which treatments are scarce. This work sought to investigate the role of miR-6721-5p in acute traumatic SCI and clarify its downstream mechanisms.</p> Methods <p>Serum miR-6721-5p was measured in 122 SCI patients and 110 trauma controls, and its diagnostic value was assessed by logistic regression and ROC analysis. In cellular experiments, BV-2 microglial cells were stimulated with LPS to assess the effects of miR-6721-5p on cell viability, inflammation, and oxidative stress. The interaction between miR-6721-5p and RTN3 was validated through luciferase reporter, RNA immunoprecipitation, and rescue experiments.</p> Results <p>Compared with the control group, patients with SCI showed markedly lower levels of miR-6721-5p. This miRNA correlated negatively with injury severity, CRP, WBC, and NLR. According to the ROC curve, it had a fair ability to discriminate SCI (AUC = 0.887). Multivariate regression analysis identified miR-6721-5p as an independent protective factor. Experiments confirmed RTN3 as a direct target of miR-6721-5p. RTN3 mRNA expression was elevated in SCI patients and inversely correlated with miR-6721-5p levels. In LPS-stimulated BV-2 cells, miR-6721-5p overexpression reversed cell viability reduction and suppressed inflammation and oxidative stress, effects that were reversed by RTN3 overexpression.</p> Conclusions <p>In patients with SCI, miR-6721-5p is markedly downregulated and may exert protective effects by targeting RTN3 to modulate microglial inflammation and oxidative stress. Results imply that miR-6721-5p holds potential as a biomarker for SCI severity, but further validation in prospective cohorts with matched trauma severity is required.</p>

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Downregulation of miR-6721-5p in the serum of patients with spinal cord injury and its role in regulating microglial inflammation via targeting RTN3

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • Yujun Zhou,
  • Liyu Sun,
  • Haitao Xu,
  • Guidi Su

摘要

Background

Spinal cord injury (SCI) remains a devastating neurological condition for which treatments are scarce. This work sought to investigate the role of miR-6721-5p in acute traumatic SCI and clarify its downstream mechanisms.

Methods

Serum miR-6721-5p was measured in 122 SCI patients and 110 trauma controls, and its diagnostic value was assessed by logistic regression and ROC analysis. In cellular experiments, BV-2 microglial cells were stimulated with LPS to assess the effects of miR-6721-5p on cell viability, inflammation, and oxidative stress. The interaction between miR-6721-5p and RTN3 was validated through luciferase reporter, RNA immunoprecipitation, and rescue experiments.

Results

Compared with the control group, patients with SCI showed markedly lower levels of miR-6721-5p. This miRNA correlated negatively with injury severity, CRP, WBC, and NLR. According to the ROC curve, it had a fair ability to discriminate SCI (AUC = 0.887). Multivariate regression analysis identified miR-6721-5p as an independent protective factor. Experiments confirmed RTN3 as a direct target of miR-6721-5p. RTN3 mRNA expression was elevated in SCI patients and inversely correlated with miR-6721-5p levels. In LPS-stimulated BV-2 cells, miR-6721-5p overexpression reversed cell viability reduction and suppressed inflammation and oxidative stress, effects that were reversed by RTN3 overexpression.

Conclusions

In patients with SCI, miR-6721-5p is markedly downregulated and may exert protective effects by targeting RTN3 to modulate microglial inflammation and oxidative stress. Results imply that miR-6721-5p holds potential as a biomarker for SCI severity, but further validation in prospective cohorts with matched trauma severity is required.