Ad-MyD88 infected MEFs: Control vs. Ad-MyD88 infected
Ontology highlight
ABSTRACT: Transcriptional profiling of Murine Embryonic Fibroblasts (MEFs) infected with Ad-MyD88 vs. Ad-GFP or mock infected. Three-condition experiment, Ad-MyD88 vs. Ad-GFP vs. Mock infected cells. Biological replicates: 3 Ad-MyD88, 3 Ad-GFP, 3 mock, independently grown and harvested. One replicate per array.
Project description:Transcriptional profiling of Bone-Marrow derived mouse Dendritic Cells (bmDCs) infected with Ad-MyD88 vs. Ad-GFP or mock infected Three-condition experiment, Ad-MyD88 vs. Ad-GFP vs. Mock infected cells. Biological replicates: 3 Ad-MyD88, 3 Ad-GFP, 3 mock, independently grown and harvested. One replicate per array.
Project description:Dysfunction of the dystrophin-glycoprotein complex (DGC) is a frequent cause of hereditary forms of muscular dystrophy. Although DGC function in maintaining skeletal muscle integrity has been well characterized, little is known about how the DGC complex is coordinately regulated at the transcriptional level. To test this hypothesis, we engineered HDAC4 stably overexpressing and control myotubes in an in vitro model of muscle differentiation. Here we present evidence that HDAC4, a neural activity-responsive histone deacetylase, is a critical transcriptional regulator of the DGC complex. We show that HDAC4 can repress multiple components of the DGC complex, including dystrophin and sarcoglycan family members in both cultured myotubes. To confirm this finding, the protein levels of core DGC complex members including dystrophin, sarcoglycan complex members, and additional dystrophin-associated proteins were evaluated in differentiated myotubes by western analysis. C2C12 mouse myotubes were infected with either a HDAC4 expressing or control (Neo) retroviruses. After stable selection, myotubes were differentiated at 90% confluency in 2% horse serum (Hyclone) for 4 days. At this time point, RNA was extracted and the two types of cells compared in a microarray analysis.
Project description:Analysis of MyD88 as a putative mediator in host-microbe-interactions MyD88-Hairpin was micro-injected in Hydra AEP embryos. The resulting Hatchling D3 showed a patchy distribution of the transgene observed by GFP. By asexual reproduction via budding and constant selection for the marker gene GFP the transgene could be driven into different cell ines. Therefore two different cultures were established. Polyps that showed no GFP-Signal anymore (control) and Polyps with both, endodermal and ectodermal transgenic cell-lines (knockdown).
Project description:Gene expression analysis of peripheral blood leukocytes (PB MNCs) to develop expression profiles that accurately reflect prior radiation exposure. Keywords: Comparative, exposure dosage, C57BI6 Murine Irradiation Studies We have made use of gene expression analysis of peripheral blood mononuclear cells (PB MNCs) to develop expression profiles that accurately reflect prior radiation exposure. Importantly, we demonstrate that expression profiles can be developed that not only predict radiation exposure in mice but also distinguish the level of radiation exposure, ranging from 50 cGy to 1000 cGy. Likewise, a molecular signature of radiation response developed solely from irradiated human patient samples can predict and distinguish irradiated human PB samples from non-irradiated samples with an accuracy of 90%, sensitivity of 85% and specificity of 94%. We further demonstrate that a radiation profile developed in the mouse can correctly distinguish PB samples from irradiated and non-irradiated human patients with an accuracy of 77%, sensitivity of 82% and specificity of 75%. Taken together, these data demonstrate that molecular profiles can be generated which are highly predictive of different levels of radiation exposure in mice and humans. Mouse Dataset only
Project description:This SuperSeries is composed of the following subset Series: GSE6871: Gene expression signatures that predict radiation exposure (human) GSE6873: Gene expression signatures that predict radiation exposure (mouse) Keywords: SuperSeries Refer to individual Series
Project description:To identify genes that may regulate distinct or overlapping functions of IRF-3 and IRF-7, primary human macrophage preparations were transduced with adenoviral vectors: Ad-GFP (control), Ad-F3 (expressing the active form of IRF-3, IRF-3 5D), or Ad-F7 (expressing the active form of IRF-7, IRF-7 D247-467) and evaluated by microarray analysis. RNA was collected 24 hours post-transduction with Ad-GFP, Ad-F3 and Ad-F7 and subjected to microarray analysis. Submited tables show the average of 7 donors.
Project description:Purpose: To investigate the changes in gene expression induced by cyclic mechanical stress (CMS) in trabecular meshwork (TM) cells. Methods: HTM cultures from three donors were plated on type I collagen-coated flexible silicone bottom plates and subjected to 15% stretching, 1 cycle per second for 6 hours. Non-stressed parallel control cultures were incubated under the same conditions in the absence of CMS. Total RNA from each culture was amplified (1 round amplification) and hybridized to Operon Human Oligo Arrays version 3.0 (35K). Control used was Universal Reference Human RNA from Stratagene. Differences in gene expression induced by CMS were analyzed using Genespring 7.2.
Project description:While recent studies of immunity have uncovered many aspects of the innate immune system, there has been precious little investigation of the cellular response to viruses in vivo. To this end, we exploited high titer adenoviral (Ad) vectors to investigate the cellular response to non-enveloped viral infection in vivo. Our results indicate a potent cellular transcriptome response early after infection, with global assessments revealing significant dysregulation in ~15% of measured transcripts derived from Ad infected tissue. Transcriptome analysis revealed a complex interplay between the innate and adaptive responses, with suppression of metabolism and mitochondrial genes akin to those observed when mice are challenged with LPS. But despite this common response profile, there were many unique aspects of the Ad dependent trancriptome response, including upregulation of several RNA regulatory mechanisms and apoptosis-related pathways, accompanied by suppression of lysosome, endocytic, Wnt, and Calcium signaling pathways. Investigations into the TLR pathway using MyD88KO mice revealed that Ad induction of the TLR, MAPK, and cytokine receptor genes are significantly dependent on MyD88, as well as five other functional gene modules (mitochondrial, RNA regulation, cell cycle and growth, extracellular, and immune response genes). Absence of MyD88 also resulted in a greatly diminished Th1 response and acute phase response at later time points, confirming the important role MyD88 plays as an anti-adenoviral immunity amplifier and regulator in vivo. However, continued activation of immune response genes in Ad infected MyD88KO mice indicates that MyD88 is not the only component of the Ad ‘sensing mechanism’ in vivo. Keywords: Infectious response, pathogen response