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Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours [RT-PCR]

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. We profiled microRNA expression in the lungs of mice infected for 24 h with Influenza A/PR/8/34 to identify microRNAs that may regulate host response to influenza infection. Mice were infected intranasally with 10e5 pfu Influenza A/PR/8/34. Lungs were isolated after 24 hours and total RNA extracted using Trizol. Equivalent quantities of RNA from 3 infected mice were pooled.

ORGANISM(S): Mus musculus

SUBMITTER: madhumati gundapuneni

PROVIDER: E-GEOD-31956 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours

Project description:This SuperSeries is composed of the following subset Series: GSE31955: Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours [Expression] GSE31956: Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours [RT-PCR] Refer to individual Series

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Project description: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, TC-1 cells stably over-expressing miR-144 were infected with influenza A for 24 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 demonstrate 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. TC-1 lung epithelial cells stably expressing miR144+miR451 or control vector were unstimulated (n=1) or infected with Influenza A/PR/8/34 (MOI=5) for 24 hours (n=3).

2012-07-31 | E-GEOD-31955 | biostudies-arrayexpress

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