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<p>Peripheral nerve injury is a salient clinical problem but lacks successful treatment schemes. Here we show the protective mechanism of hypoxia-induced Schwann cells-derived extracellular vesicles (H-EVs) carrying <i>lncRNA TNXA-PS1</i> in peripheral nerve injury. EVs isolated from RSC96 cells undergo hypoxia (H) induction. Sciatic nerve injury is induced in rats, and the animals are evaluated by Sciatic Nerve Function Index, gastrocnemius muscle mass ratio, hematoxylin &amp; eosin stain, and sensory recovery tests. <i>LncRNA TNXA-PS1</i>, <i>miR-338-3p</i>, and EGFL7 expression is tested by RT-qPCR and Western blot. Proliferation, migration, and angiogenesis of H-EVs- treated endothelial cells are assessed by CCK-8, EdU staining, transwell, and tubular formation assays. Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), NF200, P0, CD31, and vascular endothelial growth factor (VEGF) are detected. Dual luciferase assay analyzes the binding of <i>lncRNA TNXA-PS1</i>, <i>miR-338-3p</i>, and EGFL7. Results reveal that H-EVs alleviate gastrocnemius muscle atrophy, facilitate motor function recovery, and elevate NGF, BDNF, NF200, P0, CD31, and VEGF in tissues. H-EVs promote endothelial cell proliferation, migration, and tubular formation. Mechanistically, H-EVs carry <i>lncRNA TNXA-PS1</i> into endothelial cells, thus upregulating EGFL7 expression by sponging <i>miR-338-3p</i>. Collectively, H-EVs carrying <i>lncRNA TNXA-PS1</i> promote angiogenesis and nerve function recovery post sciatic nerve injury via <i>miR-338-3p</i>/EGFL7 axis.</p>

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Hypoxia-induced Schwann cells-derived extracellular vesicles carrying LncRNA TNXA-PS1 promote recovery post sciatic nerve injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月20日

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  • Zengtao Hao,
  • Zhentang Wang,
  • Jie Jia,
  • Yaxiong Wang,
  • Tao Wu,
  • Yongsheng Fan,
  • Zhiqi Huo,
  • Xinlei Zhao,
  • Shijie Yan,
  • Binghai Wang,
  • Aixinjueluo Qicheng

摘要

Peripheral nerve injury is a salient clinical problem but lacks successful treatment schemes. Here we show the protective mechanism of hypoxia-induced Schwann cells-derived extracellular vesicles (H-EVs) carrying lncRNA TNXA-PS1 in peripheral nerve injury. EVs isolated from RSC96 cells undergo hypoxia (H) induction. Sciatic nerve injury is induced in rats, and the animals are evaluated by Sciatic Nerve Function Index, gastrocnemius muscle mass ratio, hematoxylin & eosin stain, and sensory recovery tests. LncRNA TNXA-PS1, miR-338-3p, and EGFL7 expression is tested by RT-qPCR and Western blot. Proliferation, migration, and angiogenesis of H-EVs- treated endothelial cells are assessed by CCK-8, EdU staining, transwell, and tubular formation assays. Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), NF200, P0, CD31, and vascular endothelial growth factor (VEGF) are detected. Dual luciferase assay analyzes the binding of lncRNA TNXA-PS1, miR-338-3p, and EGFL7. Results reveal that H-EVs alleviate gastrocnemius muscle atrophy, facilitate motor function recovery, and elevate NGF, BDNF, NF200, P0, CD31, and VEGF in tissues. H-EVs promote endothelial cell proliferation, migration, and tubular formation. Mechanistically, H-EVs carry lncRNA TNXA-PS1 into endothelial cells, thus upregulating EGFL7 expression by sponging miR-338-3p. Collectively, H-EVs carrying lncRNA TNXA-PS1 promote angiogenesis and nerve function recovery post sciatic nerve injury via miR-338-3p/EGFL7 axis.