Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death | |
Huang, Youhua1; Huang, Xiaohong1; Yang, Ying1; Wang, Wei1; Yu, Yepin1; Qin, Qiwei1 | |
刊名 | FISH & SHELLFISH IMMUNOLOGY
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2015 | |
卷号 | 43期号:1页码:241-248 |
关键词 | RGNNV STAT3 Autophagy Necrotic cell death Viral replication |
通讯作者 | qinqw@scsio.ac.cn |
英文摘要 | The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway is an important signaling pathway activated by interferons in response to virus infection. Fish STAT3 has been demonstrated to be involved in Singapore grouper iridovirus (SGIV) infection and virus induced paraptosis, but its effects on the replication of other fish viruses still remained uncertain. Here, the roles of grouper STAT3 (Ec-STAT3) in red spotted grouper nervous necrosis virus (RGNNV) infection were investigated. The present data showed that the distribution of phosphorylated Ec-STAT3 was altered in RGNNV infected fish cells, and the promoter activity of STAT3 was significantly increased during virus infection, suggesting that STAT3 activation was involved in RGNNV infection. Using STAT3 specific inhibitor, we found that inhibition of Ec-STAT3 in vitro did not affect the transcription and protein synthesis of RGNNV coat protein (CP), however, the severity of RGNNV induced vacuolation and autophagy was significantly increased. Meanwhile, at the late stage of virus infection, RGNNV induced necrotic cell death was significantly decreased after inhibition of Ec-STAT3. Further studies indicated that Ec-STAT3 inhibition significantly increased the transcript level of autophagy related genes, including UNC-51-like kinase 2 (ULK2) and microtubule-associated protein 1 light chain 3-II (LC3-10 induced by RGNNV infection. Moreover, the expression of several pro-inflammatory factors, including TNF alpha, IL-1 beta and IL-8 were mediated by Ec-STAT3 during RGNNV infection. Together, our results not only firstly revealed that STAT3 exerted novel roles in response to fish virus infection, but also provided new insights into understanding the roles of STAT3 in different forms of programmed cell death. (C) 2014 Elsevier Ltd. All rights reserved. |
学科主题 | Fisheries; Immunology; Marine & Freshwater Biology; Veterinary Sciences |
原文出处 | 1050-4648 |
内容类型 | 期刊论文 |
源URL | [http://ir.scsio.ac.cn/handle/344004/14859] ![]() |
专题 | 南海海洋研究所_中科院海洋生物资源可持续利用重点实验室 |
作者单位 | 1.[Huang, Youhua 2.Huang, Xiaohong 3.Yang, Ying 4.Wang, Wei 5.Yu, Yepin 6.Qin, Qiwei] Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, Guangzhou 510301, Guangdong, Peoples R China 7.[Huang, Youhua 8.Huang, Xiaohong 9.Yang, Ying 10.Wang, Wei |
推荐引用方式 GB/T 7714 | Huang, Youhua,Huang, Xiaohong,Yang, Ying,et al. Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death[J]. FISH & SHELLFISH IMMUNOLOGY,2015,43(1):241-248. |
APA | Huang, Youhua,Huang, Xiaohong,Yang, Ying,Wang, Wei,Yu, Yepin,&Qin, Qiwei.(2015).Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death.FISH & SHELLFISH IMMUNOLOGY,43(1),241-248. |
MLA | Huang, Youhua,et al."Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death".FISH & SHELLFISH IMMUNOLOGY 43.1(2015):241-248. |
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