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MiR-181a Negatively Regulates Claudin-3 to Facilitate Lateolabrax maculatus Iridovirus Replication in Lateolabrax maculatus Astroglia Cells

文献类型： 外文期刊

作者： Ma, Yanping 1 ; Xu, Jingjing 1 ; Hao, Le 1 ; Wang, Gang 1 ; Huang, Wen 2 ; Liu, Zhenxing 1 ;

作者机构： 1.Guangdong Acad Agr Sci, Inst Anim Hlth, Guangzhou 510640, Peoples R China

2.Guangdong Acad Agr Sci, Collaborat Innovat Ctr, Guangzhou 510640, Peoples R China

3.Key Lab Livestock Dis Prevent Guangdong Prov, Guangzhou 510640, Peoples R China

4.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou 510640, Peoples R China

关键词： Lateolabrax maculatus iridovirus; Claudin-3; MiR-181a; virus replication

期刊名称：VIRUSES-BASEL （ 影响因子：3.5； 五年影响因子：3.7 ）

ISSN：

年卷期： 2024 年 16 卷 10 期

页码：

收录情况： SCI

摘要： Lateolabrax maculatus iridovirus (LMIV) is a variant strain of red sea bream iridovirus (RSIV), causing serious economic losses in aquaculture. Claudins (CLDNs) are major components of tight junctions (TJs) forming an important line of defense against pathogens. Our pilot miRNA-mRNA joint analysis indicated the degradation of CLDN3, as well as its interaction with miR-181a during LMIV infection. To elucidate the miR-181a/CLDN3/LMIV interactions, in vitro assays were carried out on LMB-L cells. We first confirmed that LMIV infection could decrease the expression of CLDN3, accompanied by the enhancement of permeability, suggesting the dysfunction of TJs. Contrary to the inhibition of CLDN3, the activation of miR-181a was proved, presenting a negative correlation between miR-181a and CLDN3 (Pearson r = -0.773 and p < 0.01). In addition, the influence of CLDN3 on LMIV replication was analyzed by knockdown and over-expression of CLDN3. When CLDN3 was silenced in LMB-L cells with siCLDN3-623 at 9 days post transfection (dpt), LMIV copies and titers were significantly up-regulated by 1.59-fold and 13.87-fold, respectively. By contrast, LMIV replication in LMB-L cells was reduced by 60% and 71%, post transfection with pcDNA3.1-CLDN3 over-expressed plasmid at 6 dpt and 9 dpt, respectively. Ultimately, the regulatory relationship between miR-181a and CLDN3 was further validated by dual luciferase reporter assays. Taking into account the above-described results, we proposed a "miR-181a/CLDN3/LMIV" regulatory relationship. This study provides a new insight for understanding the mechanism of LMIV replication.

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