tetano
Editor, Senior Moderator
J Biol Chem. 2017 Oct 18. pii: jbc.M117.805937. doi: 10.1074/jbc.M117.805937. [Epub ahead of print]
[h=1]MicroRNA-302a suppresses influenza A virus-stimulated interferon regulatory factor-5 expression and cytokine storm induction.[/h] Chen X[SUP]1[/SUP], Zhou L[SUP]1[/SUP], Peng N[SUP]1[/SUP], Yu H[SUP]1[/SUP], Li M[SUP]1[/SUP], Cao Z[SUP]1[/SUP], Lin Y[SUP]2[/SUP], Wang X[SUP]2[/SUP], Li Q[SUP]2[/SUP], Wang J[SUP]3[/SUP], She Y[SUP]1[/SUP], Zhu C[SUP]4[/SUP], Lu M[SUP]2[/SUP], Zhu Y[SUP]1[/SUP], Liu S[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] During influenza A virus (IAV) infection, cytokine storms play a vital and critical role in clinical outcomes. We have previously reported that microRNA (miR)-302c regulates IAV-induced IFN expression by targeting the 3'-UTR of nuclear factor kappa B (NF-κB)-inducing kinase (NIK). In the current study, we found that miR-302a, another member of miR-302 cluster, controls the IAV-induced cytokine storm. According to results from cell-based and knock-out mouse models, IAV induces a cytokine storm via interferon regulatory factor-5 (IRF-5). We also found that IAV infection upregulates IRF-5 expression and that IRF-5 in turn promotes IAV replication. Furthermore, we observed that IRF-5 is a direct target of miR-302a, which downregulated IRF-5 expression by binding its 3'-UTR. Moreover, IAV increased IRF-5 expression by downregulating miR-302a expression. Interestingly, miR-302a inhibited IAV replication. In IAV-infected patients, miR-302a expression was downregulated, whereas IRF-5 expression was upregulated. Taken together, our work uncovers and defines a signaling pathway implicated in an IAV-induced cytokine storm.
Copyright ? 2017, The American Society for Biochemistry and Molecular Biology.
[h=4]KEYWORDS:[/h] cytokine induction; influenza virus; interferon regulatory factor (IRF); microRNA (miRNA); signaling
PMID: 29046356 DOI: 10.1074/jbc.M117.805937
[h=1]MicroRNA-302a suppresses influenza A virus-stimulated interferon regulatory factor-5 expression and cytokine storm induction.[/h] Chen X[SUP]1[/SUP], Zhou L[SUP]1[/SUP], Peng N[SUP]1[/SUP], Yu H[SUP]1[/SUP], Li M[SUP]1[/SUP], Cao Z[SUP]1[/SUP], Lin Y[SUP]2[/SUP], Wang X[SUP]2[/SUP], Li Q[SUP]2[/SUP], Wang J[SUP]3[/SUP], She Y[SUP]1[/SUP], Zhu C[SUP]4[/SUP], Lu M[SUP]2[/SUP], Zhu Y[SUP]1[/SUP], Liu S[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] During influenza A virus (IAV) infection, cytokine storms play a vital and critical role in clinical outcomes. We have previously reported that microRNA (miR)-302c regulates IAV-induced IFN expression by targeting the 3'-UTR of nuclear factor kappa B (NF-κB)-inducing kinase (NIK). In the current study, we found that miR-302a, another member of miR-302 cluster, controls the IAV-induced cytokine storm. According to results from cell-based and knock-out mouse models, IAV induces a cytokine storm via interferon regulatory factor-5 (IRF-5). We also found that IAV infection upregulates IRF-5 expression and that IRF-5 in turn promotes IAV replication. Furthermore, we observed that IRF-5 is a direct target of miR-302a, which downregulated IRF-5 expression by binding its 3'-UTR. Moreover, IAV increased IRF-5 expression by downregulating miR-302a expression. Interestingly, miR-302a inhibited IAV replication. In IAV-infected patients, miR-302a expression was downregulated, whereas IRF-5 expression was upregulated. Taken together, our work uncovers and defines a signaling pathway implicated in an IAV-induced cytokine storm.
Copyright ? 2017, The American Society for Biochemistry and Molecular Biology.
[h=4]KEYWORDS:[/h] cytokine induction; influenza virus; interferon regulatory factor (IRF); microRNA (miRNA); signaling
PMID: 29046356 DOI: 10.1074/jbc.M117.805937