Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Murine primary dendritic cells: Control vs. Influenza-infected vs. polyI:C stimulated.

ABSTRACT: MIcroRNA expression profiling of primary murine splenic dendritic cells (Flt3L expanded) comparing untreated cells to cells infected with Influenza A or stimulated with polyI:C in vitro. Three-condition experiment, Influenza A/PR/8/34 virus MOI=10 vs polyI:C 30 ug/mL vs. mock treated; RNA collected after 8 hours. 3 Independent biological replicates from cells prepared on different days. One replicate per array.

ORGANISM(S): Mus musculus

SUBMITTER: Peter Askovich

PROVIDER: E-GEOD-36316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

miR-451 regulates dendritic cell cytokine responses to influenza infection.

Rosenberger Carrie M CM Podyminogin Rebecca L RL Navarro Garnet G Zhao Guo-Wei GW Askovich Peter S PS Weiss Mitchell J MJ Aderem Alan A

Journal of immunology (Baltimore, Md. : 1950) 20121119 12

MicroRNAs (miRNAs) are important posttranscriptional regulators in immune cells, but how viral infection regulates miRNA expression to shape dendritic cell (DC) responses has not been well characterized. We identified 20 miRNAs that were differentially expressed in primary murine DCs in response to the dsRNA agonist polyinosinic-polycytidylic acid, a subset of which were modestly regulated by influenza infection. miR-451 was unique because it was induced more strongly in primary splenic and lung ...[more]

PMID: 23169590

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Project description:Background: TrkB-T1 is a BDNF receptor lacking a tyrosine kinase domain that is highly expressed in astrocytes and regulates BDNF-evoked calcium transients. Previous studies indicate that downregulation of TrkB-T1 in frontal cortex may be involved in neurobiological processes underlying suicide. Methods: In a microarray screening study (N=8), we interrogated all known microRNA in the frontal cortex of suicide completers with low expression of TrkB-T1 and normal controls. These findings were validated and followed up in a larger sample of cases and controls (N=55) Functional analyses included microRNA silencing, microRNA overexpression and luciferase assays to investigate specificity and to validate interactions between differentially expressed microRNA and TrkB-T1 Results: microRNAs Hsa-miR-185* and Hsa-miR-491-3p were upregulated in suicide completers with low expression of TrkB.T1 (Pnominal: 9.10-5 and 1.8.10-4 respectively; FDR-corrected p=0.031). Bioinformatic analyses revealed five putative binding sites for the DiGeorge syndrome linked microRNA Hsa-miR-185*in the 3M-bM-^@M-^YUTR of TrkB-T1, but none for Hsa-miR-491-3P. The increase of Hsa-miR-185* in frontal cortex of suicide completers was validated then confirmed in a larger, randomly selected group of suicide completers, where an inverse correlation between Hsa-miR-185* and TrkB-T1 expression was observed ( R=-0.404; p=0.002). Silencing and overexpression studies performed in human cell lines confirmed the inverse relationship between hsa-mir-185* and trkB-T1 expression. Luciferase assays demonstrated that Hsa-miR-185* binds to sequences in the 3M-bM-^@M-^YUTR of TrkB-T1. Conclusion: These results suggest that an increase of Hsa-miR-185* expression levels regulates, at least in part, the TrkB-T1 decrease observed in the frontal cortex of suicide completers and further implicate the 3MB 22q11 region in psychopathology. The microarray analysis consists in to compare the microRNA profile of four suicide completers with low TrkB-T1 expression level and four controls. Each RNA extract was labeled with Hy3 and hybridyzed with a reference sample labeled with Hy5. The reference sample was a pool of the eight RNA samples

Dataset Information

Murine primary dendritic cells: Control vs. Influenza-infected vs. polyI:C stimulated.

Publications

miR-451 regulates dendritic cell cytokine responses to influenza infection.

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