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<p>Spinal cord injury (SCI) is a severe condition with high disability. We aimed to explore the role and mechanism of M2-EVs in SCI-induced inflammation in rats, providing novel treatment methods for SCI. Primary macrophages were differentiated into M2 macrophages. M2-EVs were extracted, followed by morphology detection and measurement of CD63, TSG101, and Calnexin. SCI rats were injected with M2-EVs, followed by assessment of hind limb motor ability, pathological changes, nerve cell morphology, and proinflammatory factor expression. LPS-stimulated spinal astrocytes were treated with M2-EVs. Cell viability, ROS levels, LDH and MDA contents, the expression of lncRNA FTX, FTX, KDM3A, and KLF3, the binding of FTX to KDM3A, and KDM3A enrichment and H3K9me2 on the KLF3 promoter were detected. Results exhibited that M2-EVs treatment increased BBB score, recovered the damaged spinal cord structure, reduced neuronal loss and proinflammatory factor expression. M2-EVs treatment increased cell viability and decreased inflammation. Mechanistically, M2-EVs delivered FTX into cells. FTX bound to KDM3A and inhibited KLF3 expression via blocking H3K9me2 demethylation. KDM3A and KLF3 overexpression partially reversed the inhibitory effect of M2-EVs on inflammation in SCI. In conclusion, M2-EVs suppress SCI inflammation by delivering FTX into cells and inhibiting the KDM3A/KLF3 axis.</p>

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Molecular Mechanism of M2 Macrophage-Derived Extracellular Vesicles in Alleviating Inflammation in Rats with Spinal Cord Injury

  • 期刊论文

  • 发表日期：

    2026年6月16日

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  • Junjie Li,
  • Shuhan Liang,
  • Jinxin Luo,
  • Yaojian Rao

摘要

Spinal cord injury (SCI) is a severe condition with high disability. We aimed to explore the role and mechanism of M2-EVs in SCI-induced inflammation in rats, providing novel treatment methods for SCI. Primary macrophages were differentiated into M2 macrophages. M2-EVs were extracted, followed by morphology detection and measurement of CD63, TSG101, and Calnexin. SCI rats were injected with M2-EVs, followed by assessment of hind limb motor ability, pathological changes, nerve cell morphology, and proinflammatory factor expression. LPS-stimulated spinal astrocytes were treated with M2-EVs. Cell viability, ROS levels, LDH and MDA contents, the expression of lncRNA FTX, FTX, KDM3A, and KLF3, the binding of FTX to KDM3A, and KDM3A enrichment and H3K9me2 on the KLF3 promoter were detected. Results exhibited that M2-EVs treatment increased BBB score, recovered the damaged spinal cord structure, reduced neuronal loss and proinflammatory factor expression. M2-EVs treatment increased cell viability and decreased inflammation. Mechanistically, M2-EVs delivered FTX into cells. FTX bound to KDM3A and inhibited KLF3 expression via blocking H3K9me2 demethylation. KDM3A and KLF3 overexpression partially reversed the inhibitory effect of M2-EVs on inflammation in SCI. In conclusion, M2-EVs suppress SCI inflammation by delivering FTX into cells and inhibiting the KDM3A/KLF3 axis.