Gga-miR-29a-3p suppresses avian reovirus-induced apoptosis and viral replication via targeting Caspase-3

• Published in: Veterinary microbiology Vol. 264; p. 109294
• Main Authors: Zhou, Linyi, Li, Jiaxin, Haiyilati, Areayi, Li, Xiaoqi, Gao, Li, Cao, Hong, Wang, Yongqiang, Zheng, Shijun J.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.2022; Elsevier BV
• Subjects: Animals; Antiviral activity; Apoptosis; Apoptosis - genetics; Arthritis; Caspase 3 - genetics; Caspase 3 - metabolism; Caspase-3; Chicken miRNAs; Chickens; Gene expression; Gene silencing; Gga-miR-29a-3p; Infections; Malabsorption; MicroRNAs; MicroRNAs - metabolism; MicroRNAs - pharmacology; miRNA; Orthoreovirus, Avian - physiology; Reovirus; Respiratory diseases; Transfection; Virus; Virus Replication - genetics; Virus; Chicken miRNAs; Gga-miR-29a-3p; Reovirus; Apoptosis
• DOI: 10.1016/j.vetmic.2021.109294
• ISSN: 0378-1135

•ARV infection increased the expression of gga-miR-29a-3p in DF-1 cells.•Gga-miR-29a-3p suppressed ARV-induced apoptosis by directly targeting Caspase 3, inhibiting viral replication.•Gga-miR-29a-3p acts as an anti-viral factor in host response to ARV infection. Avian reovirus (ARV) is an important pathogen causing multiple types of clinical diseases in chickens, including viral arthritis, chronic respiratory diseases, retarded growth, and malabsorption syndrome, leading to considerable economic losses to the poultry industry across the globe. MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression post transcriptionally by silencing or degrading their targets, thus playing important roles in the host response to pathogenic infection. However, the role of miRNAs in host response to ARV infection is still not clear. Here, we show that infection of DF-1 cells (a chicken fibroblast cell line) with ARV markedly altered the expressions of 583 chicken miRNAs(gga-miR), and that transfection of DF-1 cells with gga-miR-29a-3p, an upregulated miRNA in ARV-infected cells, significantly suppressed ARV-induced apoptosis via directly targeting Caspase-3, retarding ARV growth in cells. In contrast, knockdown of endogenous gga-miR-29a-3p in DF-1 cells by specific miRNA inhibitor enhanced ARV-induced apoptosis and increased the content and activity of caspase-3, facilitating viral growth in cells. Consistently, inhibition of Caspase-3 activity by inhibitors decreased viral titers in cell cultures. Thus, gga-miR-29a-3p plays an important antiviral role in host response to ARV infection by suppression of apoptosis via targeting Caspase-3. This information will further our understandings of how host cells combat against ARV infection by self-encoded small RNA and increase our knowledge of the role of microRNAs in host response to pathogenic infection.