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Effect of miR-144 and miR-451 expression on lung epithelial cell responses to influenza infection at 1 and 18 hours.

ABSTRACT: Antiviral responses must be regulated to rapidly defend against infection while minimizing inflammatory damage, but the mechanisms for establishing the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that negatively regulate protein levels by binding target sequences on their cognate mRNA. Here we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses, influenza, EMCV, and VSV, in primary mouse lung epithelial cells. To elucidate the mechanism whereby miR-144 increases influenza replication within lung epithelial cells, immortalized murine Type I epithelial cells (Let1 cells) stably over-expressing miR-144 were infected with influenza A for 1 or 18 hours and the transcriptional profile was compared with those of infected control cells. This systems biology approach identified the transcriptional network regulated by miR-144 and demonstrated that it controls the TRAF6/IRF7 antiviral response by post-transcriptionally suppressing TRAF6 levels. In vivo ablation of miR-144 reduced influenza replication within the lung.

ORGANISM(S): Mus musculus

PROVIDER: GSE50742 | GEO | 2013/09/11

SECONDARY ACCESSION(S): PRJNA218622

REPOSITORIES: GEO

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Effect of miR-144 and miR-451 expression on lung epithelial cell responses to influenza infection at 1 and 18 hours.

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