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

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

PROVIDER: PRJNA144999 | ENA |

REPOSITORIES: ENA

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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

2012-07-31 | E-GEOD-31957 | biostudies-arrayexpress

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

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.

2012-08-01 | GSE31955 | GEO

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

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

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

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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]

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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.

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, 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.

2013-09-11 | GSE50742 | GEO

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

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, 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. 16 RNA samples from immortalized murine Type I airway epithelial cells (Let1 cells) were analyzed using Agilent microarrays. Cells expressing miR-144, miR-451, or a vector control (GFP) were analyzed after infection with PR8 influenza virus (MOI=5) for 1 or 18 hours.

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Project description:Blood taken from a healthy human donor was used to isolate CD4CD45RO T-cells. Purified cells were stimulated with either interleukin-2 (IL-2), Interleukin-6 (IL-6) and TNF-alpha and harvested at 24 hours, 72 hours (3 days) and 144 hours (6 days) or anti-CD3 antibodies and harvested at 24 hours. These were compared to unstimulated purified CD4CD45RO T-cells harvested at 0 hours.

2008-06-01 | E-MIMR-341 | biostudies-arrayexpress

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 SubSeries listed below.

2012-08-01 | GSE31957 | GEO