Bid cleavage, cytochrome c release and caspase activation in canine coronavirus-induced apoptosis

被引:31
作者
De Martino, Luisa [1 ]
Marfe, Gabriella [2 ]
Longo, Mariangela [1 ]
Fiorito, Filomena [1 ]
Montagnaro, Serena [1 ]
Iovane, Valentina [1 ]
Decaro, Nicola [3 ]
Pagnini, Ugo [1 ]
机构
[1] Univ Naples Federico II, Dept Pathol & Anim Hlth, Fac Vet Med, I-80137 Naples, Italy
[2] Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy
[3] Univ Bari, Dept Anim Hlth & Wellbeing, I-70010 Bari, Italy
关键词
Canine coronavirus type II; Apoptosis; Caspases; PARP; Bcl-2 family members; INDUCED OLIGODENDROCYTE APOPTOSIS; PROGRAMMED CELL-DEATH; MEASURED IN-SITU; CULTURED-CELLS; DEPENDENT APOPTOSIS; VIRAL MANIPULATION; DNA FRAGMENTATION; SIGNALING PATHWAY; INFECTED-CELLS; MITOCHONDRIA;
D O I
10.1016/j.vetmic.2009.09.001
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
A previous study demonstrated that infection of a canine fibrosarcoma cell line (A-72 cells) by canine coronavirus (CCoV) resulted in apoptosis (Ruggieri et al., 2007). In this study, we investigated the cell death processes during infection and the underlying mechanisms. We found that CCoV-II triggers apoptosis in A-72 cells by activating initiator (caspase-8 and 9) and executioner (caspase-3 and -6) caspases. The proteolytic cleavage of poly(ADPribose) polymerases (PARPs) confirmed the activation of executioner caspases. Furthermore, CCoV-II infection resulted in truncated bid (tbid) translocation from the cytosolic to the mitochondrial fraction, the cytochrome c release from mitochondria, and alterations in the pro- and anti-apoptotic proteins of bcl-2 family. Our data indicated that, in this experimental model, both intrinsic and extrinsic pathways are involved. In addition, we demonstrated that the inhibition of apoptosis by caspase inhibitors did not affect CCoV replication, suggesting that apoptosis does not play a role in facilitating viral release. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:36 / 45
页数:10
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