tetano
Editor, Senior Moderator
Viruses. 2017 Nov 25;9(12). pii: E360. doi: 10.3390/v9120360.
[h=1]cfa-miR-143 Promotes Apoptosis via the p53 Pathway in Canine Influenza Virus H3N2-Infected Cells.[/h] Zhou P[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Tu L[SUP]4,[/SUP][SUP]5,[/SUP][SUP]6[/SUP], Lin X[SUP]7,[/SUP][SUP]8,[/SUP][SUP]9[/SUP], Hao X[SUP]10,[/SUP][SUP]11,[/SUP][SUP]12[/SUP], Zheng Q[SUP]13,[/SUP][SUP]14,[/SUP][SUP]15[/SUP], Zeng W[SUP]16,[/SUP][SUP]17,[/SUP][SUP]18[/SUP], Zhang X[SUP]19,[/SUP][SUP]20,[/SUP][SUP]21[/SUP], Zheng Y[SUP]22,[/SUP][SUP]23,[/SUP][SUP]24[/SUP], Wang L[SUP]25,[/SUP][SUP]26,[/SUP][SUP]27[/SUP], Li S[SUP]28,[/SUP][SUP]29,[/SUP][SUP]30[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
[h=4]KEYWORDS:[/h] apoptosis; canine influenza virus; caspase; cfa-miR-143; p53
PMID: 29186842 DOI: 10.3390/v9120360
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[h=1]cfa-miR-143 Promotes Apoptosis via the p53 Pathway in Canine Influenza Virus H3N2-Infected Cells.[/h] Zhou P[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Tu L[SUP]4,[/SUP][SUP]5,[/SUP][SUP]6[/SUP], Lin X[SUP]7,[/SUP][SUP]8,[/SUP][SUP]9[/SUP], Hao X[SUP]10,[/SUP][SUP]11,[/SUP][SUP]12[/SUP], Zheng Q[SUP]13,[/SUP][SUP]14,[/SUP][SUP]15[/SUP], Zeng W[SUP]16,[/SUP][SUP]17,[/SUP][SUP]18[/SUP], Zhang X[SUP]19,[/SUP][SUP]20,[/SUP][SUP]21[/SUP], Zheng Y[SUP]22,[/SUP][SUP]23,[/SUP][SUP]24[/SUP], Wang L[SUP]25,[/SUP][SUP]26,[/SUP][SUP]27[/SUP], Li S[SUP]28,[/SUP][SUP]29,[/SUP][SUP]30[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
[h=4]KEYWORDS:[/h] apoptosis; canine influenza virus; caspase; cfa-miR-143; p53
PMID: 29186842 DOI: 10.3390/v9120360
Free full text