tetano
Editor, Senior Moderator
Front Microbiol. 2017 Nov 7;8:2187. doi: 10.3389/fmicb.2017.02187. eCollection 2017.
[h=1]miR-194 Inhibits Innate Antiviral Immunity by Targeting FGF2 in Influenza H1N1 Virus Infection.[/h] Wang K[SUP]1[/SUP], Lai C[SUP]1[/SUP], Gu H[SUP]1[/SUP], Zhao L[SUP]1[/SUP], Xia M[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]2[/SUP], Wang X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Fibroblast growth factor 2 (FGF2 or basic FGF) regulates a wide range of cell biological functions including proliferation, angiogenesis, migration, differentiation, and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza A virus (IAV)-induced lung injury remain largely unexplored. In this study, we report that microRNA-194-5p (miR-194) expression is significantly decreased in A549 alveolar epithelial cells (AECs) following infection with IAV/Beijing/501/2009 (BJ501). We found that miR-194 can directly target FGF2, a novel antiviral regulator, to suppress FGF2 expression at the mRNA and protein levels. Overexpression of miR-194 facilitated IAV replication by negatively regulating type I interferon (IFN) production, whereas reintroduction of FGF2 abrogated the miR-194-induced effects on IAV replication. Conversely, inhibition of miR-194 alleviated IAV-induced lung injury by promoting type I IFN antiviral activities in vivo. Importantly, FGF2 activated the retinoic acid-inducible gene I signaling pathway, whereas miR-194 suppressed the phosphorylation of tank binding kinase 1 and IFN regulatory factor 3. Our findings suggest that the miR-194-FGF2 axis plays a vital role in IAV-induced lung injury, and miR-194 antagonism might be a potential therapeutic target during IAV infection.
[h=4]KEYWORDS:[/h] FGF2; H1N1; RIG-I signaling pathway; lung injury; miR-194
PMID: 29163456 PMCID: PMC5674008 DOI: 10.3389/fmicb.2017.02187
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[h=1]miR-194 Inhibits Innate Antiviral Immunity by Targeting FGF2 in Influenza H1N1 Virus Infection.[/h] Wang K[SUP]1[/SUP], Lai C[SUP]1[/SUP], Gu H[SUP]1[/SUP], Zhao L[SUP]1[/SUP], Xia M[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]2[/SUP], Wang X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Fibroblast growth factor 2 (FGF2 or basic FGF) regulates a wide range of cell biological functions including proliferation, angiogenesis, migration, differentiation, and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza A virus (IAV)-induced lung injury remain largely unexplored. In this study, we report that microRNA-194-5p (miR-194) expression is significantly decreased in A549 alveolar epithelial cells (AECs) following infection with IAV/Beijing/501/2009 (BJ501). We found that miR-194 can directly target FGF2, a novel antiviral regulator, to suppress FGF2 expression at the mRNA and protein levels. Overexpression of miR-194 facilitated IAV replication by negatively regulating type I interferon (IFN) production, whereas reintroduction of FGF2 abrogated the miR-194-induced effects on IAV replication. Conversely, inhibition of miR-194 alleviated IAV-induced lung injury by promoting type I IFN antiviral activities in vivo. Importantly, FGF2 activated the retinoic acid-inducible gene I signaling pathway, whereas miR-194 suppressed the phosphorylation of tank binding kinase 1 and IFN regulatory factor 3. Our findings suggest that the miR-194-FGF2 axis plays a vital role in IAV-induced lung injury, and miR-194 antagonism might be a potential therapeutic target during IAV infection.
[h=4]KEYWORDS:[/h] FGF2; H1N1; RIG-I signaling pathway; lung injury; miR-194
PMID: 29163456 PMCID: PMC5674008 DOI: 10.3389/fmicb.2017.02187
Free full text