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Involvement of the PI3K and ERK signaling pathways in largemouth bass virus-induced apoptosis and viral replication

文献类型： 外文期刊

作者： Huang, Xiaohong 1 ; Wang, Wei 1 ; Huang, Youhua 1 ; Xu, Liwen 3 ; Qin, Qiwei 1 ;

作者机构： 1.Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, Guangzhou 510301, Guangdong, Peoples R China

2.Univ Chinese Acad Sci, Beijing, Peoples R China

3.Chinese Acad Fishery Sci, South China Sea Fisheries Res Inst, Guangzhou 510300, Guangdong, Peoples R China

关键词： Largemouth bass;LMBV;Apoptosis;PI3K signaling pathway;ERK signaling pathway

期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.581； 五年影响因子：4.851 ）

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收录情况： SCI

摘要： Increased reports demonstrated that largemouth Bass, Micropterus salmoides in natural and artificial environments were always suffered from an emerging iridovirus disease, largemouth Bass virus (LMBV). However, the underlying mechanism of LMBV pathogenesis remained largely unknown. Here, we investigated the cell signaling events involved in virus induced cell death and viral replication in vitro. We found that LMBV infection in epithelioma papulosum cyprini (EPC) cells induced typical apoptosis, evidenced by the appearance of apoptotic bodies, cytochrome c release, mitochondrial membrane permeabilization (MMP) destruction and reactive oxygen species (ROS) generation. Two initiators of apoptosis, caspase-8 and caspase-9, and the executioner of apoptosis, caspase-3, were all significantly activated with the infection time, suggested that not only mitochondrion-mediated, but also death receptor-mediated apoptosis were involved in LMBV infection. Reporter gene assay showed that the promoter activity of transcription factors including p53, NF-kappa B, AP-1 and cAMP response element-binding protein (CREB) were decreased during LMBV infection. After treatment with different signaling pathway inhibitors, virus production were significantly suppressed by the inhibition of phosphatidylinositol 3-kinase (PI3K) pathway and extracellular-signal-regulated kinases (ERK) signaling pathway. Furthermore, LMBV infection induced apoptosis was enhanced by PI3K inhibitor LY294002, but decreased by addition of ERR inhibitor U0126. Therefore, we speculated that apoptosis was sophisticatedly regulated by a series of cell signaling events for efficient virus propagation. Taken together, our results provided new insights into the molecular mechanism of ranavirus infection. (C) 2014 Elsevier Ltd. All rights reserved.

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