无法解决的神经炎症 在慢性脊髓损伤中调节轴突再生
Andrew N Stewart1,2,3, Christopher C Bosse-Joseph2,3, Reena Kumari2,3,4
1Department of Neuroscience, University of Kentucky, Lexington, Kentucky 40536 anst265@uky.edu gensel.1@uky.edu.
概括
脊髓损伤 (SCI) 后的慢性炎症阻碍了轴突再生. 耗尽的微质细胞和巨细胞改善了轴突的生长,揭示了炎症.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 再生医学是一种再生医学.
背景情况:
- 慢性脊髓损伤 (SCI) 病变的特征是持续的微质和巨细胞积累.
- 在急性SCI中,这些免疫细胞阻碍了轴突再生;它们在慢性SCI中的作用尚不清楚.
- 持续的炎症可能是SCI后功能恢复的障碍.
研究的目的:
- 研究持续炎症对慢性SCI中轴突再生的影响.
- 确定微质和巨细胞的枯竭是否会影响已确定的SCI病变中的轴突再生.
主要方法:
- 利用PLX-5622,一个殖民地刺激因子-1受体抑制剂,在SCI后几个月内耗尽雌性小鼠的微质和巨细胞.
- 通过转录分析和免疫组织化学评估炎症标志物.
- 量化了轴突密度和神经元丰富的转录;在神经元PTEN淘汰的小鼠中测试了PLX-5622.
主要成果:
- 在慢性SCI病变中,PLX-5622治疗显著降低了炎症并增加了轴突密度.
- 治疗停止后重新填充的消耗免疫细胞,与神经元转录率升高相关.
- 在PLX-5622治疗之后,没有观察到PTEN-knockout对轴突再生的附加效应.
结论:
- 持续的炎症,由涉及CSF1的恒温机制维持,作为长期SCI中轴突再生的障碍.
- 微质细胞和巨细胞的枯竭促进了已建立的SCI病变中的轴突再生.
- 针对持续性炎症提供了一种潜在的治疗策略,以促进慢性SCI后的恢复.
关键词:
在PLX-562222中使用.在这里,我们可以使用PTEN.轴突再生的重生作用慢性脊髓损伤 慢性脊髓损伤基因治疗的基因疗法这是一种炎症炎症炎症炎症.巨细胞枯竭的消耗.逆行式的AAV是一个反向的AAV.更多相关视频
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