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Updated: Jan 13, 2026

Isolation of Tissue Extracellular Vesicles from the Liver

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富含RPS3的细胞外囊泡介导肝脊髓器官间的沟通

Peiwen Song¹, Zuomeng Wu¹, Yixiang Dong¹

¹Department of Orthopedics (Spinal Surgery), The First Affiliated Hospital of Anhui Medical University, Laboratory of Spinal and Spinal Cord Injury Regeneration and Repair, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|January 10, 2026

概括

在脊髓损伤 (SCI) 后,肝脏释放含有核糖体蛋白S3 (RPS3) 的细胞外囊泡,阻碍神经修复. 准这种肝脊髓轴和RPS3有望改善SCI后的功能恢复.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

脊髓损伤 (SCI) 破坏器官间的沟通,影响内生修复机制.
在受伤后,细胞外囊泡 (EVs) 介导脊髓和外周器官之间的通信.

研究的目的:

确定外围器官和特定分子参与抑制SCI后的神经元修复.
阐明肝脏衍生的EVs影响神经干细胞 (NSC) 和星体细胞的机制.

主要方法:

来自SCI患者的血EV的蛋白质组分析和受伤后肝脏的RNA测序.
肝脏衍生的EVs (LEVs) 的表征及其由神经细胞吸收.
研究核糖体蛋白S3 (RPS3) 和NF-κB信号传递的作用.
在体内研究涉及Kupffer细胞 (KC) 枯竭和肝脏RPS3抑制.

主要成果:

在SCI后的血EVs和LEVs中增加RPS3,LEVs针对脊髓损伤.
RPS3激活NSC和星球细胞中的NF-κB信号,抑制分化并促进神经炎症.
激活的KCs是RPS3的主要来源,放大了其肝脏的产生.
削减KCs或肝脏RPS3恢复了轴突再生,复髓化和神经功能.

结论:

存在肝脊髓轴,其中RPS3丰富的肝 EVs通过NF-κB激活抑制中枢神经系统再生.
RPS3代表了SCI的潜在预后生物标志物.
向肝脏RPS3和KC提供了SCI恢复的新治疗策略.

关键词:

星球细胞是星球细胞.轴突再生的重生过程细胞外囊泡中的细胞外囊泡.神经干细胞的神经干细胞脊髓损伤脊髓损伤脊髓损伤

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