期刊
VIRUSES-BASEL
卷 9, 期 12, 页码 -出版社
MDPI
DOI: 10.3390/v9120360
关键词
cfa-miR-143; canine influenza virus; apoptosis; p53; caspase
类别
资金
- National Natural Science Foundation of China [31672563]
- National Key Research and Development Program of China [2016YFD0501004]
- Special Fund for Agro-scientific Research in the Public Interest [201303042]
- Guangdong Provincial Key Laboratory of Prevention and Control for Severe Clinical Animal Diseases [2013A061401013]
MicroRNAs regulate multiple aspects of the host response to viral infection. This study verified that the expression of cfa-miR-143 was upregulated in vivo and in vitro by canine influenza virus (CIV) H3N2 infection. To understand the role of cfa-miR-143 in CIV-infected cells, the target gene of cfa-miR-143 was identified and assessed for correlations with proteins involved in the apoptosis pathway. A dual luciferase reporter assay showed that cfa-miR-143 targets insulin-like growth factor binding protein 5 (Igfbp5). Furthermore, a miRNA agomir and antagomir of cfa-miR-143 caused the downregulation and upregulation of Igfbp5, respectively, in CIV-infected madin-darby canine kidney (MDCK) cells. This study demonstrated that cfa-miR-143 stimulated p53 and caspase3 activation and induced apoptosis via the p53 pathway in CIV H3N2-infected cells. In conclusion, CIV H3N2 induced the upregulation of cfa-miR-143, which contributes to apoptosis via indirectly activating the p53-caspase3 pathway.
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