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神经元-小胶质细胞EphA4/ephrin通路调控小胶质细胞介导的缺血后炎性损伤

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神经元-小胶质细胞EphA4/ephrin通路调控小胶质细胞介导的缺血后炎性损伤
Neuron-microglia communication via EphA4/ephrin signaling pathway regulates post-ischemic inflammatory injury mediated by microglia
上传时间:2019/4/18 15:12:44    作者:魏慧星,陈萍萍,吴钢,杨锦珊|下载

魏慧星,陈萍萍,吴钢,杨锦珊*
(福建医科大学附属第一医院神经内科,福州350000)
Wei Huixing, Chen Pingping, Wu Gang, Yang Jinshan*
(Department of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou 35000, China)

摘要:目的  观察神经元-小胶质细胞间EphA4/ephrin 信号通路在脑缺血后的炎性损伤中的作用及机制。方法 建立神经元-小胶质细胞混合培养体系和糖氧剥夺再复氧(oxygen-glucose deprivation and reperfusion, OGD/R)模型,使用预聚集化的EphA4-Fc激动小胶质细胞ephrin配体,检测OGD/R后的细胞凋亡、小胶质细胞增殖和亚型极化以及小胶质细胞功能改变。 结果  EphA4受体高表达于原代神经元,与对照组相比,预聚集化EphA4-Fc干预加重OGD/R导致的细胞凋亡,促进小胶质细胞增殖以及向M1型(促炎型)极化(炎症表型)。结论 神经元-小胶质细胞间EphA4/ephrin 信号通路通过调控小胶质细胞亚型极化参与脑缺血后的炎性损伤的过程。
脑缺血;炎性损伤;EphA4/ephrin通路;小胶质细胞亚型极化
〔中图分类号〕R743.4             〔文献标识码〕A             DOI:10.16705/ j. cnki. 1004-1850. 2019. 01. 004
Abstract: Objective  To investigate the role of neuron-microglia communication via EphA4/ephrin signaling pathway in inflammatory injury after ischemia and its mechanism. Methods Neuron-microglia co-culture system was constructed, as well as the oxygen-glucose deprivation and reperfusion (OGD/R) model was established. Pre-clustered EphA4-Fc was used as the agonist of microglial ephrin ligand. Then EphA4/ephrin signaling between neuron and microglia, namely OGD/R induced apotosis, microglial proliferation, polarization and function changes were analyzed. Results EphA4 receptor was highly expressed in primary neurons. Comparing to control group, pre-clustered EphA4-Fc intervention aggravated OGD/R-induced apoptosis as well as promoted microglial proliferation and its polarization to M1  type (inflammatory phenotype). Conclusion EphA4/ephrin signaling pathway between neuron and microglia was involved in the post-ischemic inflammatory injury by regulating polarization of microglia subtype.
Cerebral ischemia; inflammatory injury; EphA4/ephrin signaling pathway; microglia subtype polarization

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