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Effect of the ribonuclease binase on the proteome of A549 cell infected by influenza A(H1N1pdm09) virus

ABSTRACT: Ribonucleases (RNases) of different origin demonstrate antiviral effects that are mediated by the direct RNase action on RNA species and can also involve signal transduction modulation. To reveal cellular targets and explain the mechanisms underlying the antiviral effect employed by the small extracellular ribonuclease of Bacillus pumilus (binase) both in vitro and in vivo, a shotgun proteomic analysis of influenza A virus (H1N1pdm09)-infected A549 cells upon binase treatment, was performed.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Raihan Shah Mahmud

PROVIDER: PXD014809 | JPOST Repository | Mon Jul 29 00:00:00 BST 2019

REPOSITORIES: jPOST

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Project description:Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection. Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection.

			Action	DRS
	All_list1.qsession	Other
	All_list2.qsession	Other
	C1_list1_1.wiff	Wiff
	C1_list1_1.wiff.scan	Wiff
	C1_list1_2.wiff	Wiff

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Effect of the ribonuclease binase on the proteome of A549 cell infected by influenza A(H1N1pdm09) virus

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