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SRP043160
Mus musculus
16 Downloadable Samples
Ion Torrent Proton
Description
We previously found that the SF3A mRNA splicing complex was required for a robust innate immune response; SF3A acts in part by inhibiting the production of a negatively acting splice form of the TLR signaling adaptor MyD88. Here we inhibit SF3A1 using RNAi and subsequently perform an RNAseq study to identify the full complement of genes and splicing events regulated by SF3A in murine macrophages. Surprisingly, SF3A has substantial specificity for mRNA splicing events in innate immune signaling pathways compared to other pathways, affecting the splicing of many genes in the TLR signaling pathway to modulate the innate immune response. Overall design: RNAseq was used to monitor the effects of SF3A1 siRNA-mediated knockdown in murine macrophages. Three biological replicates were used for each of the four treatment combinations (with/without siRNA, with/without LPS). The first replicates for each combination were each sequenced in two runs, which were combined in the analysis.
Publication Title
Regulation of toll-like receptor signaling by the SF3a mRNA splicing complex.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Ion Torrent Proton
Description
Splenocytes from lymphoreplete, unmanipulated mice were analyzed for basal mRNA levels. We hypothesized, based on previous data from our lab and others, that many cytokine/inflammatory response genes would show an increase from na誰ve CD5lo<CD5hi<Virtual memory. Overall design: mRNA was analyzed from mouse splenocytes separated into na誰ve CD5lo, na誰ve CD5hi, and virtual memory cells. Mice were lymphoreplete and unmanipulated.
Publication Title
Virtual memory T cells develop and mediate bystander protective immunity in an IL-15-dependent manner.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 248 Downloadable Samples
- Illumina HiSeq 2000
Description
Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality, is primarily caused by prolonged exposures to cigarette smoke (CS) and the disease may persist or progress even after smoking cessation. To provide novel insight the mechanisms of COPD development we investigated temporal patterns of lung transcriptome expression in response to chronic CS exposure that also persist following CS cessation, using next generation sequencing techniques. Whole lung RNA-seq data was analyzed from C57Bl/6 mice exposed to CS for 1 day, 7 days, 1 month, 3 months, 6 months, and 9 months as well as for 6 months followed by 3 months of cessation. Age-matched littermate mice exposed to ambient air were used as control (AC). Differential gene expression and pathway analyses revealed consistent upregulation of genes involved in glutathione metabolism, a pathway previously implicated in lung responses to chronic CS and in COPD, that was reversible upon cessation. In addition, novel patterns in mouse-model pathways such as pyrimidine metabolism and phosphatidylinositol signaling system and have been recognized. Genes in these pathways encoding for enzymes controlling metabolic functions were significantly altered by CS exposures and were associated with congruent abnormalities in contemporaneous plasma metabolomic profiles. The bioinformatics integration of lung tissue genomics and plasma metabolomics uncovered that changes in lung gene expression induced by CS exposures are translated in systemic metabolic signatures, with potential implication in the development of COPD. Overall design: Whole transcriptome profiling of air control vs cigarette smoke-exposed mice at each of 6 timepoints from 1 day to 9 months of exposure, including a stop smoking group exposed to 6 months of CS followed by 3 months of ambient air recovery. Each treatment-by-time experimental group contains 5 biological replicates. 3 samples were discarded for quality reasons.
Publication Title
Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject, Time
View Samples- Mus musculus
- 31 Downloadable Samples
- Ion Torrent Proton
Description
In this study we demonstrate that the lung mononuclear phagocyte system comprises three interstitial macrophages (IMs), as well as alveolar macrophages (AMs), dendritic cells and few extravascular monocytes. Through cell sorting and RNAseq analysis we were able to identify transcriptional similarities and differences between the three pulmonary IM subtypes, with reference to the more well-characterized alveolar macrophage Overall design: Pulmonary Interstitial and Alveolar macrophages were FACS sorted from the lungs of steady state 8-10 week old B6 mice, in triplicate. Extracted RNA was examined by RNAsequencing. The tar archive GSE94135_jakubzick_2019*tar available at the foot of this page contains the supplementary processed data used for comparisons with data in GSE132911. Data were processed as described in GSE132911.
Publication Title
Three Unique Interstitial Macrophages in the Murine Lung at Steady State.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Ion Torrent Proton
Description
Macrophages (MF) have been shown to contribute to fibrogenesis, however the underlying mechanisms and specific MF subsets involved remain unclear. Lung MF can be divided into two subsets: Siglec-Fhi resident alveolar MF and CD11bhi MF that primarily arise from immigrating monocytes. RNA-seq analysis was performed to compare these MF subsets during fibrosis. CD11bhi MF, not Siglec-Fhi MF, expressed high levels of pro-fibrotic chemokines and growth factors. Overall design: C56BL/6 WT mice were treated intratracheally with bleomycin. 8 days later, CD64+Mertk+ MF were sorted into Siglec-F(high) and CD11b(high) subsets. SiglecF(high) MF from naïve mice were also sorted. RNA was isolated and RNA-seq was performed to compare MF subsets.
Publication Title
Deletion of c-FLIP from CD11b<sup>hi</sup> Macrophages Prevents Development of Bleomycin-induced Lung Fibrosis.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 104 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Clinical heterogeneity of esrtrogen receptor-negative, progesterone receptor-negative [ER(-)/PR(-)] breast cancer (BC) suggests biological heterogeneity. We performed gene expression analysis of primary BCs and BC cell lines to identify the underlying biology of ER(-)/PR(-) disease, define subsets, and identify potential therapeutic targets.
Publication Title
An estrogen receptor-negative breast cancer subset characterized by a hormonally regulated transcriptional program and response to androgen.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Macaca mulatta
- 32 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
The mucosa that lines the respiratory and gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Using the simian immunodeficiency virus (SIV) rhesus macaque model, we have performed a comparative analysis of host gene expression in the lung and GI mucosa in response to SIV infection and antiretroviral therapy.
Publication Title
Enhanced innate antiviral gene expression, IFN-α, and cytolytic responses are predictive of mucosal immune recovery during simian immunodeficiency virus infection.
Sample Metadata Fields
Specimen part
View Samples- Macaca mulatta, Homo sapiens
- 13 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Cell line, Treatment
View Samples- Macaca mulatta
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Macaca mulatta
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples