This SuperSeries is composed of the SubSeries listed below.
Translational regulation of specific mRNAs controls feedback inhibition and survival during macrophage activation.
Specimen part, Time
View SamplesWhen macrophages encounter pathogens, they transiently induce an orchestrated cascade of pro- and anti-inflammatory genes. We systematically analyzed the contribution of translational regulation to the early phase of macrophage activation. While the expression of most cytokines is regulated by changes in mRNA levels, de-repression of translation was found to permit expression of many feedback inhibitors of the inflammatory response. This includes NF-kB inhibitors (IkBd, IkBz, Nr4a1, Ier3), a p38 MAPK antagonist (Dusp1) and post-transcriptional suppressors of cytokine expression (TTP and Zc3h12a). Ier3 is tightly co-regulated with TNF at the level of mRNA abundance and translation. Macrophages lacking Ier3 show reduced survival upon activation, indicating that induction of Ier3 is required to protect macrophages from lipopolysaccharide-induced cell death. Our analysis reveals an important role of translational regulation in the resolution of inflammation and macrophage survival.
Translational regulation of specific mRNAs controls feedback inhibition and survival during macrophage activation.
Specimen part
View SamplesWhen macrophages encounter pathogens, they transiently induce an orchestrated cascade of pro- and anti-inflammatory genes. To obtain a precise picture of transcriptome-wide mRNA expression patterns, we performed RNA-Seq of total RNA at a high temporal resolution during the first two hours of macrophage activation. We systematically analyzed the contribution of translational regulation to the early phase of macrophage activation. While the expression of most cytokines is pre-dominanatly regulated by changes in mRNA levels, de-repression of translation was found to permit expression of many feedback inhibitors of the inflammatory response. Overall design: Expression profiles of LPS-treated Raw264.7 cells (0, 15, 30, 45, 60, 75, 90 and 120 min after stimulation) were generated by deep sequencing using Illumina HiSeq 2000.
Translational regulation of specific mRNAs controls feedback inhibition and survival during macrophage activation.
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View SamplesIllumina RNA sequencing to study DEGs between freshly isolated and emigrated skin T cells Overall design: skin T cell RNA profile of freshly isolated T cells and emigrated T cells under IL-2, IL-4, TGF-beta and IL-2, IL-15 cytokine condition
The cytokine environment influence on human skin-derived T cells.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Anti-inflammatory properties of alpha- and gamma-tocopherol.
Sex
View SamplesWe established the transcriptional profile of brain aging and examine the global effects of vitamin E supplementation on age-related alterations in expression in the aged mouse brain.
Anti-inflammatory properties of alpha- and gamma-tocopherol.
Sex
View SamplesTo investigate the global effects of vitamin E supplementation on heart aging, we used high-density oligonucleotide arrays to measure transcriptional alterations in 30-month-old B6C3F1 mice supplemented with - and -tocopherol since middle age (15 months).
Anti-inflammatory properties of alpha- and gamma-tocopherol.
Sex
View SamplesInjured skeletal muscle regenerates, but with age or in muscular dystrophies, muscle is replaced by fat. Upon injury, muscle-resident fibro/adipogenic progenitors (FAPs) proliferated and gave rise to adipocytes. These FAPs dynamically produced primary cilia, structures that transduce intercellular cues such as Hedgehog (Hh) signals. Genetically removing cilia from FAPs inhibited intramuscular adipogenesis, both after injury and in a mouse model of Duchenne muscular dystrophy. Blocking FAP ciliation also enhanced myofiber regeneration after injury and reduced myofiber size decline in the muscular dystrophy model. Hh signaling through FAP cilia regulated the expression of TIMP3, a secreted metalloproteinase inhibitor, that inhibited MMP14 to block adipogenesis. A pharmacological mimetic of TIMP3 blocked the conversion of FAPs into adipocytes, pointing to a strategy to combat fatty degeneration of skeletal muscle. We conclude that ciliary Hh signaling by FAPs orchestrates the regenerative response to skeletal muscle injury. Overall design: Transcriptomic profiling using RNAseq was performed on RNA derived from a bipotent, progenitor cell population, called fibro/adipogenic progenitors (FAPs), purified from tibialis anterior muscle 3 days post glycerol injury. Two populations of cells were sequenced, one from wild type muscle (FAP-ctrl) and another from cells in which cilia, using a floxed Ift88 allele, were conditionally deleted (FAP-no cilia). A total of five FAP-ctrl and 3 FAP-no cilia samples were used. The TruSeq Stranded Total RNA Library Prep Kit (Ilumina) was used to generate the library, which was subsequently sequenced using an Illumina 2500 SE 50bp platform and aligned to the GRCm38.78 whole genome using STAR RNAseq aligner. Individual read counts were normalized to the geometric mean read count across all samples using DEseq. Sequencing yielded ~314 million total reads with an average read depth of ~34.9 million reads per sample.
Ciliary Hedgehog Signaling Restricts Injury-Induced Adipogenesis.
Specimen part, Cell line, Subject
View SamplesExpression data were generated on 136 subjects from the COPDGene study using Affymetrix microarrays. Multiple linear regression with adjustment for covariates (gender, age, body mass index, family history, smoking status, pack years) was used to identify candidate genes and Ingenuity Pathway Analysis was used to identify candidate pathways.
Peripheral blood mononuclear cell gene expression in chronic obstructive pulmonary disease.
Sex, Specimen part
View SamplesGenome wide gene expression profile of the lrx1 root hair mutant and the suppressor mutations lrx1 rol1-1 and lrx1 rol1-2.
The Arabidopsis root hair cell wall formation mutant lrx1 is suppressed by mutations in the RHM1 gene encoding a UDP-L-rhamnose synthase.
Age, Specimen part
View Samples