Dysregulation of Ephrin receptor and PPAR signaling pathways in neural progenitor cells infected by Zika virus.
Dysregulation of Ephrin receptor and PPAR signaling pathways in neural progenitor cells infected by Zika virus.
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DOI：
10.1080/22221751.2020.1818631
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发表时间：
2020-12
影响因子：
13.2
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Thulasi Raman SN;Latreille E;Gao J;Zhang W;Wu J;Russell MS;Walrond L;Cyr T;Lavoie JR;Safronetz D;Cao J;Sauve S;Farnsworth A;Chen W;Shi PY;Wang Y;Wang L;Rosu-Myles M;Li X
寨卡病毒（ZIKV）感染是一种严重的公共威胁，约70个国家和地区报告了病例。ZIKV感染最严重的后果之一是婴儿先天性小头畸形。先天性小头畸形被认为是由发育中的胎儿脑中的神经祖细胞（NPC）感染引起的。然而，小头畸形发展的分子和细胞机制仍有待充分阐明。在这项研究中，我们采用定量蛋白质组学，以确定蛋白质表达谱发生在病毒复制的NPC。蛋白质表达变化的生物信息学分析导致了广泛的细胞信号通路的鉴定。具体而言，参与神经发生和胚胎发育的途径明显改变，沿着与细胞周期，细胞凋亡，脂质代谢和氧化应激相关的途径。值得注意的是，通过定量蛋白质组学揭示并通过qPCR阵列验证的肝配蛋白受体和PPAR信号传导途径的差异调节强调了在疾病发展中探索这些途径的必要性。总的来说，这些结果表明ZIKV诱导的发病机制涉及复杂的病毒-宿主反应;这里报道的发现可以帮助阐明ZIKV诱导的小头畸形和ZIKV在NPC中复制的机制。
Zika virus (ZIKV) infection is a serious public threat with cases reported in about 70 countries and territories. One of the most serious consequences of ZIKV infection is congenital microcephaly in babies. Congenital microcephaly has been suggested to result from infection of neural progenitor cells (NPCs) in the developing fetal brain. However, the molecular and cellular mechanisms underlying microcephaly development remains to be fully elucidated. In this study, we employed quantitative proteomics to determine protein expression profile that occur during viral replication in NPCs. Bioinformatics analysis of the protein expression changes resulted in the identification of a wide range of cell signaling pathways. Specifically, pathways involved in neurogenesis and embryonic development were markedly altered, along with those associated with cell cycle, apoptosis, lipid metabolism and oxidative stress. Notably, the differential regulation of Ephrin Receptor and PPAR signaling pathways, as revealed by quantitative proteomics and validated by qPCR array, underscores the need to explore these pathways in disease development. Collectively, these results indicate that ZIKV-induced pathogenesis involves complex virus-host reactions; the findings reported here could help shed light on the mechanisms underlying ZIKV-induced microcephaly and ZIKV replication in NPCs.
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