Autor: |
Yuhong Pan, Wenjun Cai, Anchun Cheng, Mingshu Wang, Shun Chen, Juan Huang, Qiao Yang, Ying Wu, Di Sun, Sai Mao, Dekang Zhu, Mafeng Liu, Xinxin Zhao, Shaqiu Zhang, Qun Gao, Xumin Ou, Bin Tian, Zhongqiong Yin, Renyong Jia |
Jazyk: |
angličtina |
Rok vydání: |
2022 |
Předmět: |
|
Zdroj: |
Veterinary Research, Vol 53, Iss 1, Pp 1-13 (2022) |
Druh dokumentu: |
article |
ISSN: |
1297-9716 |
DOI: |
10.1186/s13567-022-01070-9 |
Popis: |
Abstract Duck Tembusu virus (DTMUV) is a pathogenic flavivirus that has caused enormous economic losses in Southeast Asia. Our previous study showed that DTMUV could induce duck embryo fibroblast (DEF) apoptosis, but the specific mechanism was not clear. In this study, we confirmed that DTMUV could induce the apoptosis of DEFs by DAPI staining and TUNEL staining. Furthermore, we found that the expression levels of cleaved-caspase-3/7/8/9 were significantly upregulated after DTMUV infection. After treatment of cells with an inhibitor of caspase-8 or caspase-9, DTMUV-induced apoptosis rates were significantly decreased, indicating that the caspase-8-mediated death receptor apoptotic pathway and caspase-9-mediated mitochondrial apoptotic pathway were involved in DTMUV-induced apoptosis. Moreover, we found that DTMUV infection not only caused the release of mitochondrial cytochrome C (Cyt C) and the downregulation of the apoptosis-inhibiting protein Bcl-2 but also reduced the mitochondrial membrane potential (MMP) and the accumulation of intracellular reactive oxygen species (ROS). Key genes in the mitochondrial apoptotic pathway and death receptor apoptotic pathway were upregulated to varying degrees, indicating the activation of the mitochondrial apoptosis pathway and death receptor apoptosis pathway. In conclusion, this study clarifies the molecular mechanism of DTMUV-induced apoptosis and provides a theoretical basis for revealing the pathogenic mechanism of DTMUV infection. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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