Mus musculus
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ABSTRACT:
PROVIDER: PRJNA155283 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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
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
Project description:Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours
| PRJNA144999 | ENA
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.
2013-09-11 | E-GEOD-50742 | biostudies-arrayexpress
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
Project description:Effect of miR-144/miR451 expression on TC-1 lung epithelial cell responses to influenza infection for 24 hours [RT-PCR]
| PRJNA155285 | ENA
Project description:Effect of miR-144 and miR-451 expression on lung epithelial cell responses to influenza infection at 1 and 18 hours.
| PRJNA218622 | ENA
Project description:The regulation of host defense against influenza A viruses (IAVs) infection has attracted much attention, especially for type I interferon (IFN)-mediated innate response. Here we revealed that miR-93 expression was significantly downregulated in Alveolar epithelial type II cells (AT2) upon IAVs infection through RIG-I/JNK pathway. Inhibition of miR-93 was found to suppress host antiviral innate response by facilitating type I IFN effector signaling, and JAK1 was identified to be directly targeted by miR-93. Importantly, in vivo administration of miR-93 antagomiR significantly inhibited miR-93 expression and markedly suppressed IAVs infection, which in turn prevented the death of IAVs infected mice. Hence, the inducible downregulation of miR-93 suppress IAVs infection by upregulation IFN-JAK-STAT effector pathway, and in vivo inhibition of miR-93 bears considerable therapeutic potential for suppressing IAVs infection. The miRNA profiling in mice lung was measured at 24 and 36 hours after gave each mouse 50µl of influenza A (50 µl of 10-6 TCID50/µl) via retropharyngeal instillation. Three mice were performed at each time (24 or 36 hours) and RNA from different donors was mixed before determination.
2015-06-22 | E-GEOD-70125 | biostudies-arrayexpress
Project description:Background: The in vivo gene response associated with hyperthermia and subsequent return to homeostasis or development of heat illness is poorly understood. Early activation of gene networks in the heat stress response is likely to lead to the systemic inflammation, multi-organ functional impairment, and other pathophysiological states characteristic of heat illness. Here, we perform an unbiased global characterization of the multi-organ gene response using an in vivo model of heat stress in the conscious rat. Results: Rats were subjected to elevated temperatures until implanted thermal probes indicated a maximal core temperature of 41.8 M-BM-0C (Tc,Max). Liver, lung, kidney, and heart were harvested at Tc,Max, 24 hours, and 48 hours after heat stress in groups of experimental animals and time-matched controls kept at ambient temperature. Clinical chemistries suggested abnormal function in liver, kidney, and lung at Tc,Max, and cardiac histopathology at 48 hours supported persistent cardiac damage in 3 out of 6 animals. Microarray analysis identified 78 differentially expressed genes common to all 4 organs at Tc,Max (i.e., the consensus heat stress response). Gene set enrichment analysis of gene ontology terms identified 25 biological processes in 4 general gene ontology categories: protein folding, regulation of apoptosis, response to cytokines, and transcriptional responses. Functional analysis clustering of the 78 differentially expressed genes in the consensus heat stress response also identified functional categories of protein folding and regulation of apoptosis. Self-organizing maps identified gene-specific signatures corresponding to protein folding disorders specific to only heat-stressed rats with histopathologic evidence of cardiac injury at 48 hours. Enrichment analysis of differentially expressed proteins in heat-injured hearts at 48 hours corroborated gene enrichment analysis results. Quantitative proteomics analysis by iTRAQ demonstrated that differential protein expression was not comparable to transcript expression at Tc,Max and 24 hours. However, the profile of differentially expressed proteins closely matched the transcriptomic profile in heat-injured animals at 48 hours. Pathway analysis at both the transcript and protein levels supported catastrophic deficits in energetics and cellular metabolism, chronic proteotoxic response, and activation of the unfolded protein response. Calculation of protein super-saturation scores demonstrated an increased propensity of proteins to aggregate in the hearts of heat-injured animals at 48 hours, consistent with accumulation of misfolded proteins. Conclusions: Global transcriptomic and proteomic analysis identified networks of genes and proteins initiating an unfolded protein response, metabolic dysfunction, and mitochondrial energy crisis in animals with histopathologic evidence of persistent heat injury, providing the basis for a systems-level physiological model of heat illness and recovery. To induce the pathophysiological effects of heat stress, conscious rats were placed in an incubator at 37M-BM-:C and their core temperature was monitored. Animals were sacrificed when their core temperature reached 41.8M-BM-:C (Tc,Max), or they were returned to their normal housing environment and were allowed to recover for up to 24 or 48 hours prior to sacrifice. Time-matched controls were euthanized at times corresponding to Tc,Max, 24 hours, and 48 hours. For each condition n=6 for a total of 36 animals. Four tissues (liver, lung, kidney and heart) were analyzed from each animal for a total of 144 arrays; however a few arrays did not pass QC therefore only 140 are reported here: 34 liver, 35 lung, 36 kidney, or 35 heart.
2015-01-14 | E-GEOD-56740 | biostudies-arrayexpress