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Bta-miR-98 Suppresses Replication of Caprine Parainfluenza Virus Type 3 Through Inhibiting Apoptosis by Targeting Caspase-3

文献类型： 外文期刊

作者： Li, Jizong 1 ; Zhong, Chunyan 1 ; Liao, Zheng 1 ; Mao, Li 1 ; Li, Wenliang 1 ; Sun, Min 1 ; Liu, Maojun 1 ; Ji, Xinqin 1 ; L 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med, Key Lab Vet Diag, Key Lab Vet Biol Engn & Technol,Minist Agr, Nanjing, Peoples R China

2.Linyi Univ, Sch Pharm, Linyi, Shandong, Peoples R China

3.Jiangsu Univ, Sch Food & Biol Engn, Inst Life Sci, Zhenjiang, Jiangsu, Peoples R China

4.Guizhou Univ, Coll Anim Sci, Guiyang, Peoples R China

5.Jiangsu Acad Agr Sci, Key Lab Food Qual & Safety Jiangsu Prov, State Key Lab Breeding Base, Nanjing, Peoples R China

关键词： Caprine parainfluenza virus type 3; miRNA; bta-miR-98; caspase-3; apoptosis

期刊名称：FRONTIERS IN IMMUNOLOGY （ 影响因子：7.561； 五年影响因子：7.624 ）

ISSN： 1664-3224

年卷期： 2020 年 11 卷

页码：

收录情况： SCI

摘要： Caprine parainfluenza virus type 3 (CPIV3) is an emerging respiratory pathogen that affects the sheep and goat industry in China and possibly other countries around the world. Accumulating evidence suggests that microRNAs play important roles in regulating virus-host interactions and can suppress or facilitate viral replication. In this study, we showed that CPIV3 infection induced apoptosis in Madin-Darby bovine kidney (MDBK) cells, as determined by morphological changes and flow cytometry. Caspase activity and the expression of pro-apoptotic genes further indicated that CPIV3 induced apoptosis by activating both the intrinsic and extrinsic pathways. We also demonstrated the involvement of bta-microRNA-98 (bta-miR-98) in regulating CPIV3-induced apoptosis. Bta-miR-98 was downregulated in MDBK cells infected with CPIV3. Overexpression of bta-miR-98 significantly decreased the activities of caspase-3, -8, and -9. Conversely, inhibition of bta-miR-98 had completely opposite effects. Furthermore, our data showed that bta-miR-98 markedly affected CPIV3 replication by regulating apoptosis. Importantly, we found that bta-miR-98 modulated CPIV3-induced apoptosis by targeting caspase-3, an effector of apoptosis. Collectively, our results may suggest that CPIV3 infection induced apoptosis and downregulated the levels of bta-miR-98, and this miRNA regulated viral replication through effected apoptosis. This study contributes to our understanding of the molecular mechanisms underlying CPIV3 pathogenesis.

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