红藻氨酸
拮抗剂
小胶质细胞
促炎细胞因子
癫痫
神经炎症
和平号-155
医学
炎症
内科学
内分泌学
小RNA
神经科学
生物
谷氨酸受体
生物化学
基因
受体
作者
Fang Huang,Yiyun Cheng,Haijuan Luo,Zhouyi Rong,Yanfang Li,Ping Lu,Xiaowen Ye,Weiyan Huang,Ziguo Qi,Xiuying Li,Baoying Cheng,Xintian Wang,Yi Yao,Yunwu Zhang,Weihong Zheng,Honghua Zheng
出处
期刊:Neuroimmunomodulation
[S. Karger AG]
日期:2019-01-01
卷期号:26 (2): 67-76
被引量:17
摘要
Neuroinflammation is an important contributor to the development of seizures and epilepsy. Micro-RNA-155 (miR-155) plays a critical role in immunity and -inflammation. This study aims to explore the function of miR-155 and miR-155-mediated inflammation in epilepsy.About 8-week-old male C57BL/6 mice were administered an intraperitoneal injection (i.p.) of kainic acid (KA) (15 mg/kg) or saline. The mice in the KA group developing acute seizure were further subjected to intracerebroventricular injection (i.c.v.) of antagomir negative control (NC) or miR-155 antagomir. Animal behavior was observed according to Racine's scale, and electroencephalographs were recorded. Primary microglia were cultured and treated with antagomir NC or antagomir. Whole-cell electrophysiological recording was conducted to detect the spontaneous EPSCs and IPSCs in the neurons treated with different conditioned medium from those microglia. miR-155 were detected by qRT-PCR in those models, as well as in the brain or blood from epileptic patients and healthy controls.miR-155 was abundantly expressed in glial cells compared with neurons, and its expression was markedly elevated in the brain of epilepsy patients and KA-induced seizure mice. Silencing miR-155 attenuated KA-induced seizure, abnormal electroencephalography, proinflammatory cytokine expression, and microglia morphology change. Moreover, conditioned media from KA-treated microglia impaired neuron excitability, whereas conditioned media from KA and miR-155 antagomir co-treated microglia had no such effects. Finally, miR-155 levels were significantly higher in the blood of epilepsy patients than those of healthy controls.These findings demonstrate that aberrant upregulation of miR-155 contributes to epileptogenesis through inducing microglia neuroinflammation.
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