Involvement of the mitogen-activated protein kinase pathway in soft-shelled turtle iridovirus-induced apoptosis |
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Authors: | Youhua Huang Xiaohong Huang Jia Cai Fuzhou Ye Qiwei Qin |
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Institution: | (1) Key Laboratory of Marine Bio-resources Sustainable Utilization, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou, 510301, China;(2) State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, 135 West Xingang Road, Guangzhou, 510275, China; |
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Abstract: | Iridoviruses are large DNA viruses that infect invertebrates and poikilothermic vertebrates, and result in significant economic
losses in aquaculture production, and drastic declines in amphibian populations. Soft-shelled turtle iridovirus (STIV) is
the causative agent of severe systemic diseases in farm-raised soft-shelled turtles (Trionyx sinensis). In the present study, the mechanisms of STIV-induced cell death and the roles of the mitogen-activated protein kinase (MAPK)
signaling pathway were investigated. STIV infection evoked typical apoptosis in fish cells, as demonstrated by the formation
of apoptotic bodies, positive terminal deoxynucleotidyl transferase-mediated nicked-end labeling, and caspase-3 activation.
The translocation of cytochrome c from mitochondria to cytoplasm, and caspase-9 activation suggested that a mitochondria-mediated pathway was involved in STIV-induced
apoptosis. Moreover, MAPK pathways, including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK signaling were activated during STIV infection. Using specific inhibitors, we found that
MAPK signaling molecules, including ERK, JNK and p38 MAPK, were important for virus release, whereas, only ERK and p38 MAPK
were involved in STIV-induced apoptosis by modulating caspase-3 activity. Taken together, our findings shed light on the roles
of the MAPK signaling pathway in iridovirus-induced apoptosis and virus replication, which provides new insights into understanding
iridovirus–host interaction. |
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