期刊
MARINE BIOTECHNOLOGY
卷 23, 期 2, 页码 294-307出版社
SPRINGER
DOI: 10.1007/s10126-021-10023-w
关键词
Epinephelus coioides; miR-122; SGIV; Apoptosis
资金
- National Natural Science Foundation of China [31930115, 31772877]
- National key research and development plan subject [2019YFD0900801, 2020YFD0901100]
- foundation of Key Laboratory of Tropical Marine Bio-resources and Ecology, Chinese Academy of Sciences [2019011008]
- Hainan Key Laboratory of Tropical Marine Biotechnology [LTMB201902]
The study revealed that SGIV infection can up-regulate the expression of E. coioides miR-122, and the up-regulation of miR-122 can affect the activation of inflammatory factors, the activity of AP-1 and NF-kappa B, as well as cell apoptosis to regulate viral replication and proliferation.
In mammals, mature miR-122 is 22 nucleotides long and can be involved in regulating a variety of physiological and biological pathways. In this study, the expression profile and effects of grouper Epinephelus coioides miR-122 response to Singapore grouper iridovirus (SGIV) infection were investigated. The sequences of mature microRNAs (miRNAs) from different organisms are highly conserved, and miR-122 from E. coioides exhibits high similarity to that from mammals and other fish. The expression of miR-122 was up-regulated during SGIV infection. Up-regulation of miR-122 could significantly enhance the cytopathic effects (CPE) induced by SGIV, the transcription levels of viral genes (MCP, VP19, LITAF and ICP18), and viral replication; reduce the expression of inflammatory factors (TNF-a, IL-6, and IL-8), and the activity of AP-1 and NF-kappa B, and miR-122 can bind the target gene p38 alpha MAPK to regulate the SGIV-induced cell apoptosis and the protease activity of caspase-3. The results indicated that SGIV infection can up-regulate the expression of E. coioides miR-122, and up-regulation of miR-122 can affect the activation of inflammatory factors, the activity of AP-1 and NF-kappa B, and cell apoptosis to regulate viral replication and proliferation.
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