Enterovirus 71 leads to abnormal mitochondrial dynamics in human neuroblastoma SK-N-SH cells.
Enterovirus 71 leads to abnormal mitochondrial dynamics in human neuroblastoma SK-N-SH cells.
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DOI：
10.1016/j.virusres.2023.199267
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发表时间：
2024-01-02
期刊：
影响因子：
5
通讯作者：
Wang, Huan
中科院分区：
文献类型：
--
作者：
Zhang, Wanling;Yang, Haiyan;Liu, Zhengyun;Wang, Shengyu;Chen, Tianyang;Song, Hong;Xu, Yunbin;Li, Fajin;Luo, Guo;Wang, Huan
本研究旨在阐明EV71感染过程中线粒体动力学在人神经母细胞瘤SK-N-SH细胞中的作用。EV71诱导SK-N-SH细胞内线粒体形态和动力学的改变，可能损害线粒体功能并导致神经系统功能障碍。恢复适当的线粒体动力学可能是对抗EV71感染的一种有前途的方法。EV71是一种引起手足口病的重要病原体，与脑干脑炎、无菌性脑膜炎和急性弛缓性麻痹等严重神经系统并发症有关。虽然线粒体动力学在调节许多病毒复制中的作用已得到确认，但其在EV71中的具体作用仍不清楚。本研究旨在阐明EV71感染过程中线粒体动力学在人神经母细胞瘤SK-N-SH细胞中的作用。利用激光共聚焦显微镜和透射电镜，我们观察到EV71感染诱导线粒体伸长和嵴结构损伤，同时加速线粒体运动。此外，我们发现EV71感染后，动力蛋白相关蛋白1 （Drp1）和视神经萎缩蛋白1 （Opa1）的表达减少，Mitofusion 2 （Mfn2）的表达增加。值得注意的是，EV71直接刺激线粒体活性氧（ROS）的产生，导致线粒体膜电位和ATP水平下降。值得注意的是，褪黑激素（一种有效的线粒体保护剂）的应用通过恢复Drp1的表达来抑制EV71的复制。这些发现共同表明，EV71诱导SK-N-SH细胞内线粒体形态和动力学的改变，可能损害线粒体功能并导致神经系统功能障碍。恢复适当的线粒体动力学可能是对抗EV71感染的一种有前途的方法。
This study aimed to elucidate the role of mitochondrial dynamics in human neuroblastoma SK-N-SH cells during EV71 infection. EV71 induces alterations in mitochondrial morphology and dynamics within SK-N-SH cells, potentially impairing mitochondrial function and contributing to nervous system dysfunction. The restoration of proper mitochondrial dynamics may hold promise as a prospective approach to counteract EV71 infection. EV71, a significant pathogen causing hand-foot-mouth disease, is associated with severe neurological complications such as brain stem encephalitis, aseptic meningitis, and acute flaccid paralysis. While the role of mitochondrial dynamics in regulating the replication of numerous viruses is recognized, its specific involvement in EV71 remains unclear. This study aimed to elucidate the role of mitochondrial dynamics in human neuroblastoma SK-N-SH cells during EV71 infection. Utilizing laser confocal microscopy and transmission electron microscopy, we observed that EV71 infection induced mitochondrial elongation and damage to cristae structures, concurrently accelerating mitochondrial movement. Furthermore, we identified the reduction in the expression of dynamin-related protein 1 (Drp1) and optic atrophy protein 1 (Opa1) and the increased expression of Mitofusion 2 (Mfn2) upon EV71 infection. Notably, EV71 directly stimulated the generation of mitochondrial reactive oxygen species (ROS), leading to a decline in mitochondrial membrane potential and ATP levels. Remarkably, the application of melatonin, a potent mitochondrial protector, inhibited EV71 replication by restoring Drp1 expression. These findings collectively indicate that EV71 induces alterations in mitochondrial morphology and dynamics within SK-N-SH cells, potentially impairing mitochondrial function and contributing to nervous system dysfunction. The restoration of proper mitochondrial dynamics may hold promise as a prospective approach to counteract EV71 infection.
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DOI：
10.3390/v15071518
发表时间：
2023-07-07
期刊：
Viruses
影响因子：
--
作者：
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期刊：
Biochimica et biophysica acta
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Siddiqui A
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