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Involvement of miR-15a in G0/G1 Phase Cell Cycle Arrest Induced by Porcine Circovirus Type 2 Replication

文献类型： 外文期刊

作者： Quan, Rong 1 ; Wei, Li 1 ; Zhu, Shanshan 1 ; Wang, Jing 1 ; Cao, Yongchang; Xue, Chunyi; Yan, Xu 1 ; Liu, Jue 2 ;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, 9 Shuguang Garden Middle Rd, Beijing 100097, Peoples R China

2.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, 9 Shuguang Garden Middle Rd, Beijing 100097, Peoples R

期刊名称：SCIENTIFIC REPORTS （ 影响因子：4.379； 五年影响因子：5.133 ）

ISSN： 2045-2322

年卷期： 2016 年 6 卷

页码：

收录情况： SCI

摘要： Many viruses exploit the host cell division cycle to favour their own growth. Here we demonstrated that porcine circovirus type 2 (PCV2), which is a major causative agent of an emerging and important swine disease complex, PCV2-associated diseases, caused G0/G1 cell cycle arrest through degradation of cyclin D1 and E followed by reduction of retinoblastoma phosphorylation in synchronized PCV2-infected cells dependent upon virus replication. This induction of G0/G1 cell cycle arrest promoted PCV2 replication as evidenced by increased viral protein expression and progeny virus production in the synchronized PCV2-infected cells. To delineate a mechanism of miRNAs in regulating PCV2-induced G0/G1 cell cycle arrest, we determined expression levels of some relevant miRNAs and found that only miR-15a but not miR-16, miR-21, and miR-34a was significantly changed in the PCV2-infected cells. We further demonstrated that upregulation of miR-15a promoted PCV2-induced G0/G1 cell cycle arrest via mediating cyclins D1 and E degradation, in which involves PCV2 growth. These results reveal that G0/G1 cell cycle arrest induced by PCV2 may provide favourable conditions for viral protein expression and progeny production and that miR-15a is implicated in PCV2-induced cell cycle control, thereby contributing to efficient viral replication.

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