Duck enteritis virus infection suppresses viability and induces apoptosis and endoplasmic reticulum stress in duck embryo fibroblast cells via the regulation of Ca2+

文献类型： 外文期刊

第一作者： Zhang, Yangzi

作者： Zhang, Yangzi;Hu, Andong;Zhang, Piao;Yang, Xia;Wen, Ming;Zhang, Yangzi;Wang, Xuan;Wu, Yutong;Wen, Zhengchang;Hu, Andong;Zhang, Piao;Yang, Xia;Wen, Ming

作者机构：

关键词： apoptosis; duck enteritis virus; endoplasmic reticulum stress; ethylenediaminetetraacetic acid

期刊名称：JOURNAL OF VETERINARY MEDICAL SCIENCE （ 影响因子：1.049； 五年影响因子：1.099 ）

ISSN： 0916-7250

年卷期： 2021 年 83 卷 3 期

页码：

收录情况： SCI

摘要： Duck viral enteritis (DVE) is a lethal viral disease caused by duck enteritis virus (DEV) via an unknown mechanism. This study explores the relationship between Chinese standard challenge strain DEV (DEV-CSC)-induced apoptosis and endoplasmic reticulum stress (ERS) in duck embryo fibroblast (DEF) cells. Here we examined changes in Ca2+ concentration, cell proliferation, apoptosis, and the differential expression of C/EBP homologous protein (CHOP), glucose regulatory protein 78 (GRP78), and activating transcription factor 6 (ATF6) in infected cells. The results revealed that DEV-CSC infection significantly decreased Ca2+ concentration, suppressed cell viability, and induced apoptosis in DEF cells. Further experiments also demonstrated that DEV-CSC infection significantly upregulates CHOP, GRP78, and ATF6 expression. In addition, we show that the addition of ethylenediaminetetraacetic acid (EDTA) reverses the induction of apoptosis and the ERS mediated inhibition of cell viability in DEF cells associated with DEV-CSC infection. Therefore, we can conclude that infection with DEV-CSC induces apoptosis and ERS reducing the viability of DEF cells via the regulation of Ca2+. These findings may provide a new target for the treatment of DVE.

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