神经炎症
微泡
小胶质细胞
神经突
神经元
外体
细胞生物学
神经科学
慢性创伤性脑病
小RNA
化学
医学
体外
免疫学
生物
炎症
生物化学
基因
脑震荡
伤害预防
环境卫生
毒物控制
作者
Zhenyu Yin,Zhaoli Han,Tianpeng Hu,Shishuang Zhang,Xintong Ge,Shan Huang,Lu Wang,Jinwen Yu,Wenzhu Li,Yan Wang,Dai Li,Jing Zhao,Yifeng Wang,Yan Zuo,Ying Li,Xiaodong Kong,Fanglian Chen,Ping Lei
标识
DOI:10.1016/j.bbi.2019.11.004
摘要
Neuroinflammation is a characteristic pathological change of acute neurological deficit and chronic traumatic encephalopathy (CTE) after traumatic brain injury (TBI). Microglia are the key cell involved in neuroinflammation and neuronal injury. The type of microglia polarization determines the direction of neuroinflammation. MiR-21-5p elevated in neurons and microglia after TBI in our previous research. In this study, we explore the influence of miR-21-5p for neuroinflammation by regulating microglia polarization. In this study, PC12 and BV2 used to instead of neuron and microglia respectively. The co-cultured transwell system used to simulate interaction of PC12 and BV2 cells in vivo environment. We found that PC12-derived exosomes with containing miR-21-5p were phagocytosed by microglia and induced microglia polarization, meanwhile, the expression of miR-21-5p was increased in M1 microglia cells. Polarization of M1 microglia aggravated the release of neuroinflammation factors, inhibited the neurite outgrowth, increased accumulation of P-tau and promoted the apoptosis of PC12 cells, which formed a model of cyclic cumulative damage. Simultaneously, we also got similar results in vivo experiments. PC12-derived exosomes with containing miR-21-5p is the essential of this cyclic cumulative damage model. Therefore, regulating the expression of miR-21-5p or the secretion of exosomes may be an important novel strategy for the treatment of neuroinflammation after TBI.
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