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在神经病痛条件下,巨细胞通过细胞外囊泡与神经元进行神经元通信
Francesca Picco1, Lynda Zeboudj1, Silvia Oggero1
1Wolfson Sensory, Pain and Regeneration Centre, King's College London, London, United Kingdom.
Heliyon
|January 15, 2025
概括
促炎性巨细胞释放含有microRNA-155 (miR-155) 的细胞外囊泡 (EV),这些囊泡转移到神经元,增加疼痛信号. 在临床前模型中,抑制这种EV转移可以减少神经病痛.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 周围神经损伤通过神经元和免疫细胞的变化引起神经病痛.
- 来自背部根 (DRG) 神经元的细胞外囊 (EV) 促进巨细胞的积累和疼痛信号.
- 巨细胞还通过与神经元相互作用,导致神经病痛.
研究的目的:
- 研究巨细胞衍生的EVs在将microRNA-155 (miR-155) 转移到感觉神经元中的作用.
- 确定这种转移对基因表达和疼痛信号的影响.
- 评估针对神经性疼痛的这种途径的治疗潜力.
主要方法:
- 骨髓衍生的巨细胞 (BMDMs) 用于产生含有miR-155.5的EV.
- 培养的感觉神经元被暴露在这些电子电路中,以评估吸收和分子变化.
- 在临床前的神经病痛疼痛模型中,注射了EVs和miR-155对抗体.
- 测量了Ship1和IL-6表达和机械过敏度的变化.
主要成果:
- BMDMs释放含有miR-155的EV,这些EV被感官神经元吸收.
- EV介导的miR-155转移抑制了Ship1的表达,并增加了神经元中的IL-6水平.
- 内注射BMDM衍生的EVs局部化到DRG.
- 用miR-155治疗的抗体载的EVs上调Ship1,下调IL-6和减轻神经病痛.
结论:
- 亲炎性巨细胞在神经病变条件下将含有miR-155的EV送往感官神经元.
- 这种细胞间沟通有助于DRG中前感受性IL-6的表达.
- 向巨细胞衍生的EV和miR-155代表了神经病痛的潜在治疗策略.
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