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神经原始细胞和发育中的神经元衍生的细胞外囊不同调节微质激活.

Tsung-Lang Chiu1, Hsin-Yi Huang2, Hock-Kean Liew2

  • 1Division of Neurosurgery, Neuro-Medical Scientific Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.

International journal of molecular sciences
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概括

神经前代细胞和发育中的神经元释放细胞外囊泡,激活微质细胞. 这种由Toll-like受体7介导的激活会影响微质细胞的发育,并促进多巴胺基神经元的存活.

关键词:
这就是MAPKs.在 NF-κBB 中.收费类受体 7 收费类受体 7发育中的神经元.细胞外囊泡中的细胞外囊泡.微质细胞中的微质细胞神经前代细胞的神经前代细胞

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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:

  • 在大脑发育过程中,小质细胞从激活到非激活状态的过渡.
  • 控制这种微质发育过渡的机制尚不清楚.
  • 细胞外囊泡 (EVs) 中介细胞间的通信.

研究的目的:

  • 研究来自神经原生细胞 (NPC) 和发育中的神经元在微质激活中的EVs的作用.
  • 为了阐明参与EV介导微质调制的信号通路.
  • 确定这些相互作用对神经元生存的影响.

主要方法:

  • 长期的神经元培养系统与NPC和微质细胞.
  • 电动汽车的隔离和特征.
  • 在微质中分析细胞因子表达 (TNF-α,IL-1β,IL-6) 和信号通路 (MAPK,NF-κB).
  • 药理上抑制了托尔类受体7 (TLR7) 的作用.
  • 评估多巴胺基神经元存活率.

主要成果:

  • 来自NPC和不成熟神经元的EVs与成熟神经元的EVs相比,诱导了更高的微质炎症细胞因子表达.
  • NPC/未成熟的神经元衍生的EV激活了微质中的MAPK和NF-κB信号.
  • TLR7调解了EV诱导的NF-κB和MAPK通路的激活.
  • 由NPC/未成熟神经元EVs条件下的微质促进了多巴胺基神经元的存活.

结论:

  • NPC和发育中的神经元利用EV来调节微质激活状态和功能.
  • TLR7信号传递是EV介导微质反应的关键途径.
  • 这种基于EV的交叉语音在支持发育的神经元群体方面发挥着作用.