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Proteome Analysis in a Mammalian Cell line Reveals that PLK2 is Involved in Avian Metapneumovirus Type C (aMPV/C)-Induced Apoptosis.
Viruses ( IF 3.8 ) Pub Date : 2020-03-28 , DOI: 10.3390/v12040375 Rong Quan , Li Wei , Lei Hou 1 , Jing Wang 1 , Shanshan Zhu 1 , Zixuan Li 1 , Moran Lv 1 , Jue Liu 1
Viruses ( IF 3.8 ) Pub Date : 2020-03-28 , DOI: 10.3390/v12040375 Rong Quan , Li Wei , Lei Hou 1 , Jing Wang 1 , Shanshan Zhu 1 , Zixuan Li 1 , Moran Lv 1 , Jue Liu 1
Affiliation
Avian metapneumovirus subtype C (aMPV/C) causes an acute respiratory disease that has caused serious economic losses in the Chinese poultry industry. In the present study, we first explored the protein profile in aMPV/C-infected Vero cells using iTRAQ quantitative proteomics. A total of 921 of 7034 proteins were identified as significantly altered by aMPV/C infection. Three selected proteins were confirmed by Western blot analysis. Bioinformatics GO analysis revealed multiple signaling pathways involving cell cycle, endocytosis, and PI3K-Akt, mTOR, MAPK and p53 signaling pathways, which might participate in viral infection. In this analysis, we found that PLK2 expression was upregulated by aMPV/C infection and investigated whether it contributed to aMPV/C-mediated cellular dysfunction. Suppressing PLK2 attenuated aMPV/C-induced reactive oxygen species (ROS) production and p53-dependent apoptosis and reduced virus release. These results in a mammalian cell line suggest that high PLK2 expression correlates with aMPV/C-induced apoptosis and viral replication, providing new insight into the potential avian host cellular response to aMPV/C infection and antiviral targets.
更新日期：2020-04-20
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