Xiao Xiang, Du Yu, Zhuangzhuang Li, Jelke J Fros, Jianchao Wei, Ke Liu, Zongjie Li, Donghua Shao, Beibei Li, Jeroen Kortekaas, Monique M van Oers, Zhiyong Ma, Gorben P Pijlman, Yafeng Qiu
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引用次数: 0
摘要
日本脑炎病毒(JEV)是一种具有神经侵袭性和神经侵入性的黄病毒,可引起病毒性脑炎,严重威胁畜牧业的发展和人类健康。DNA 甲基化是病毒致病过程中的主要表观遗传修饰,但 DNA 甲基化如何影响 JEV 感染仍是未知数。在这里,我们展示了与模拟感染小鼠相比,JEV 感染小鼠大脑中的全基因组 DNA 甲基化图谱。JEV能明显增加JEV感染小鼠大脑中DNA甲基化的整体水平。共鉴定出 14781 个差异甲基化区域相关基因(DMGs)。随后,KEGG通路分析表明,DNA甲基化可调节紧密连接信号通路,从而可能影响血脑屏障(BBB)的通透性。我们证明,在体外透孔试验中,紧密连接基因 Afdn 启动子的高甲基化抑制了 AFDN 的表达,并增加了小鼠脑微血管内皮细胞(bEnd.3)的单层渗透性。总之,这项研究揭示了 DNA 甲基化在小鼠日本脑炎模型中会增加,而调节 Afdn 的表达会促进 BBB 的通透性。
Japanese encephalitis virus-induced DNA methylation contributes to blood-brain barrier permeability by modulating tight junction protein expression.
Japanese encephalitis virus (JEV) is a neurotropic and neuroinvasive flavivirus causing viral encephalitis, which seriously threatens the development of animal husbandry and human health. DNA methylation is a major epigenetic modification involved in viral pathogenesis, yet how DNA methylation affects JEV infection remains unknown. Here, we show genome-wide DNA methylation profiles in the brains of JEV-infected mice compared to mock-infected mice. JEV can significantly increase the overall DNA methylation levels in JEV-infected mouse brains. A total of 14,781 differentially methylated regions associated genes (DMGs) have been identified. Subsequently, KEGG pathway analysis suggested that DNA methylation modulates the tight junction signaling pathway, which can potentially impact the permeability of the blood-brain barrier (BBB). We demonstrate that hypermethylation of the tight junction gene Afdn promoter inhibited AFDN expression and increased monolayer permeability of mouse brain microvascular endothelial (bEnd.3) cells in an in vitro transwell assay. Collectively, this study reveals that DNA methylation is increased in a murine Japanese encephalitis model and that modulation of Afdn expression promotes BBB permeability.
期刊介绍:
The Journal of Neuroinflammation is a peer-reviewed, open access publication that emphasizes the interaction between the immune system, particularly the innate immune system, and the nervous system. It covers various aspects, including the involvement of CNS immune mediators like microglia and astrocytes, the cytokines and chemokines they produce, and the influence of peripheral neuro-immune interactions, T cells, monocytes, complement proteins, acute phase proteins, oxidative injury, and related molecular processes.
Neuroinflammation is a rapidly expanding field that has significantly enhanced our knowledge of chronic neurological diseases. It attracts researchers from diverse disciplines such as pathology, biochemistry, molecular biology, genetics, clinical medicine, and epidemiology. Substantial contributions to this field have been made through studies involving populations, patients, postmortem tissues, animal models, and in vitro systems.
The Journal of Neuroinflammation consolidates research that centers around common pathogenic processes. It serves as a platform for integrative reviews and commentaries in this field.