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斜带石斑鱼 miR-122 在 SGIV 感染和复制中的作用。

The Roles of Epinephelus coioides miR-122 in SGIV Infection and Replication.

机构信息

Joint Laboratory of Guangdong Province and Hong Kong Regions on Marine Bioresource Conservation and Exploitation, Guangdong Laboratory for Lingnan Modern Agriculture, College of Marine Sciences, South China Agricultural University, Guangdong Province, 510642, Guangzhou, People's Republic of China.

出版信息

Mar Biotechnol (NY). 2021 Apr;23(2):294-307. doi: 10.1007/s10126-021-10023-w. Epub 2021 Feb 11.

Abstract

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-κB, and miR-122 can bind the target gene p38α 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-κB, and cell apoptosis to regulate viral replication and proliferation.

摘要

在哺乳动物中,成熟的 miR-122 长 22 个核苷酸,可以参与调节多种生理和生物途径。在这项研究中,我们研究了斜带石斑鱼 Epinephelus coioides miR-122 对新加坡石斑鱼虹彩病毒(SGIV)感染的表达谱和作用。不同生物体成熟 microRNAs(miRNAs)的序列高度保守,而来自 E. coioides 的 miR-122 与哺乳动物和其他鱼类的 miR-122 具有高度相似性。在 SGIV 感染过程中,miR-122 的表达上调。miR-122 的上调可以显著增强 SGIV 引起的细胞病变效应(CPE)、病毒基因(MCP、VP19、LITAF 和 ICP18)的转录水平和病毒复制;降低炎症因子(TNF-a、IL-6 和 IL-8)的表达以及 AP-1 和 NF-κB 的活性,miR-122 可以结合靶基因 p38α MAPK 来调节 SGIV 诱导的细胞凋亡和 caspase-3 的蛋白酶活性。结果表明,SGIV 感染可以上调斜带石斑鱼 miR-122 的表达,而 miR-122 的上调可以影响炎症因子的激活、AP-1 和 NF-κB 的活性以及细胞凋亡,从而调节病毒的复制和增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ee0/8032594/7615b110fc32/10126_2021_10023_Fig1_HTML.jpg

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