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Roles of bovine viral diarrhea virus envelope glycoproteins in inducing autophagy in MDBK cells

机译: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

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摘要

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.
机译:巨自噬(自噬)是一种进化上保守的控制过程,可维持真核细胞中的细胞稳态。自噬主要起着适应性作用,以降解功能障碍的蛋白质并清除因病原体,病毒或微生物感染,营养缺乏和内质网(ER)应激引起的受损细胞器。在先前的研究中,我们显示了牛病毒性腹泻病毒(BVDV)NADL感染诱导的自噬,并且在MDBK细胞中感染后12小时显着提高了自噬相关基因Beclin1和ATG14的表达水平。但是,尚不清楚控制自噬活性的具体机制。在这里,我们调查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-LC3点状阳性细胞的百分比以及Beclin1和ATG14的表达水平。而El的过表达不会影响自噬活动。总体而言,这些发现表明病毒包膜糖蛋白E-rns和E2参与诱导自噬,并为病毒感染细胞中自噬的调控提供了机械原理。 (C)2014 Elsevier Ltd.保留所有权利。

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