Roles of bovine viral diarrhea virus envelope glycoproteins in inducing autophagy in MDBK cells
Roles of bovine viral diarrhea virus envelope glycoproteins in inducing autophagy in MDBK cells
复制标题
牛病毒性腹泻病毒包膜糖蛋白在诱导 MDBK 细胞自噬中的作用
DOI：
10.1016/j.micpath.2014.09.011
复制
发表时间：
2014-11-01
影响因子：
3.8
通讯作者：
Chen, Chuangfu
中科院分区：
文献类型：
--
作者：
Fu, Qiang;Shi, Huijun;Chen, Chuangfu
自噬是真核细胞中维持细胞内稳态的一种进化上保守的控制过程。自噬主要发挥适应性作用，降解功能失调的蛋白质，并清理受损的细胞器，以应对病原体，病毒或微生物感染，营养剥夺和内质网（ER）应激。在先前的研究中，我们发现牛病毒性腹泻病毒（BVDV）NADL感染诱导MDBK细胞自噬，并在感染后12 h显著升高自噬相关基因Beclin 1和ATG 14的表达水平。然而，涉及控制自噬活性的具体机制仍不清楚。在这里，我们研究了BVDV NADL包膜糖蛋白过表达对诱导自噬的影响。结果表明，慢病毒介导的病毒包膜糖蛋白E-rns和E2过表达增加了自噬体的形成、GFP-LC 3斑点阳性细胞的百分比以及Beclin 1和ATG 14的表达水平。而El过表达不影响自噬活性。总的来说，这些发现表明，病毒包膜糖蛋白E-rns和E2参与诱导自噬，并提供了一个机制的见解，在病毒感染的细胞自噬的调节。(C)2014爱思唯尔有限公司版权所有。
Macroautophagy (autophagy) is an evolutionarily conserved control process that maintains cellular homeostasis in eukaryotic cells. Autophagy principally serves an adaptive role to degrade dysfunctional proteins and to clean damaged organelles in response to pathogenic, viral, or microbial infection, nutrient deprivation and endoplasmic reticulum (ER) stress. In previous study, we showed bovine viral diarrhea virus (BVDV) NADL infection induced autophagy and significantly elevated the expression levels of autophagy-related genes, Beclin1 and ATG14, at 12 h post-infection in MDBK cells. However, the specific mechanisms involved in controlling autophagic activity remain unclear. Here, we investigate the effects of BVDV NADL envelope glycoproteins overexpression on inducing autophagy. The results show that viral envelope glycoproteins E-rns and E2 overexpression mediated by lentivirus increase the formation of autophagosome, the percentage of GFP-LC3 puncta-positive cells and the expression levels of Beclin1 and ATG14. Whereas El overexpression doesn't affect autophagic activity. Collectively, these findings suggest that the viral envelope glycoproteins E-rns and E2 are involved in inducing autophagy, and provide a mechanistic insight into the regulation of autophagy in viral infected cells. (C) 2014 Elsevier Ltd. All rights reserved.