This SuperSeries is composed of the SubSeries listed below.
Surgery-Induced Weight Loss Is Associated With the Downregulation of Genes Targeted by MicroRNAs in Adipose Tissue.
Sex, Specimen part, Subject
View SamplesMolecular mechanisms associated with pathophysiological variations in adipose tissue (AT) are not fully recognized. The main aim of this study was to identify novel candidate genes and miRNAs that may contribute to the pathophysiology of hyperplastic AT. Therefore, wide gene and microRNA (miRNA) expression patterns were assessed in subcutaneous AT of 16 morbidly obese women before and after surgery-induced weight loss. Validation of microarray data was performed by quantitative real-time PCR both longitudinally (n=25 paired samples) and cross-sectionally (25 obese vs. 26 age-matched lean women). Analyses in macrophages and differentiated human adipocytes were also performed to try to comprehend the associations found in AT. 5,018 different probe sets identified significant variations in gene expression after treatment (adjusted p-value<0.05). A set of 16 miRNAs also showed significant modifications. Functional analysis revealed changes in genes and miRNAs associated with cell cycle, development and proliferation, lipid metabolism, and the inflammatory response. Canonical affected pathways included TREM1, PI3K, and EIF2 signaling, hepatic stellate cell activation, and mitochondrial function. Increased expression of SLC27A2, ELOVL6, FASN, GYS2, LGALS12, PKP2, ACLY, and miR-575, as well as decreased FOS, EGFL6, PRG4, AQP9, DUSP1, RGS1, EGR1, SPP1, LYZ, miR-130b, miR-221, and miR-155, were further validated. The clustering of similar expression patterns for gene products with related functions revealed molecular footprints, some of them described for the first time, which elucidate changes in biological processes after the surgery-induced weight loss.
Surgery-Induced Weight Loss Is Associated With the Downregulation of Genes Targeted by MicroRNAs in Adipose Tissue.
Sex, Specimen part, Subject
View SamplesWe used RNA sequencing to study gene expression in lymph node derived DCs from anaphylactic mice sensitized intranasally with the major peach allergen Pru p 3, during the acute reaction phase, induced intraperitoneally. In total, 237 genes changed significantly, 181 showing at least two-fold changes. Almost three quarters of these increased during anaphylaxis Overall design: 5 Female Balb/c mice aged 4-5 weeks, were sensitized to peach using intranasally administered Pru p 3 in combination with LPS and challenged intraperitoneally as described previously . 5 Littermates, treated with intranasally administered PBS (instead of Pru p 3 and LPS), and later given an intraperitoneal challenge as per the anaphylactic mice, were used for comparison.
Transcriptional Profiling of Dendritic Cells in a Mouse Model of Food-Antigen-Induced Anaphylaxis Reveals the Upregulation of Multiple Immune-Related Pathways.
Sex, Cell line, Treatment, Subject
View SamplesA great number of studies have investigated changes induced by morphine exposure in gene expression using several experimental models. In this study, we examined gene expression changes during chronic exposure to morphine during maturation and differentiation of zebrafish CNS.
Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine: identification of new genes associated with neuronal function and mu opioid receptor expression.
Treatment
View SamplesDocetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells.
Suppression of acquired docetaxel resistance in prostate cancer through depletion of notch- and hedgehog-dependent tumor-initiating cells.
Specimen part, Cell line
View SamplesThe combination of defined factors with small molecules targeting epigenetic factors is a strategy that has been shown to enhance optimal derivation of human iPSCs and could be used for therapeutic and regenerative medicine applications. In this study, we showed that a new first-in-class dual G9a/DNMT inhibitor CM272 compound improves the standard four-factor reprogramming efficiency of human fibroblast. The use of CM272 facilitates the generation of iPSC with only two factors, OCT4 and SOX2, allowing the removal of potentially oncogenic factors such as cMYC or KLF4. Taking a closer look at the early events occurring during cell reprogramming we demonstrated that treatment with our G9a/DNMT dual inhibitor induces heterochromatin relaxation, facilitates the engagement of OCT4 and SOX2 transcription factors to the genome and promotes mesenchymal to epithelial transition during cell reprogramming. Thus, the use of this new G9a/DNMT dual inhibitor compound may represent an interesting alternative for improving cell reprogramming.
Reversible dual inhibitor against G9a and DNMT1 improves human iPSC derivation enhancing MET and facilitating transcription factor engagement to the genome.
Sex, Specimen part, Disease, Cell line
View SamplesCombined treatment with NRG-1 and DMSO led to efficient differentiation of iPS into mature ventricular-like cardiac cells, which were capable of preserving cardiac function and tissue viability when transplanted into a mouse model of myocardial infarction.
Neuregulin-1β induces mature ventricular cardiac differentiation from induced pluripotent stem cells contributing to cardiac tissue repair.
Sex
View SamplesThe transcription factor GATA2 regulates chemotherapy resistance in prostate cancer. We report a novel GATA2 transcriptional program that has implications for chemotherapy resistance disease and aggressiveness in castration resistant prostate cancer. Overall design: Examination of the transcriptional network changes induced in human Ch-CRPC cell lines by two shRNA mediated knock down of GATA2 versus random shRNA control
A targetable GATA2-IGF2 axis confers aggressiveness in lethal prostate cancer.
No sample metadata fields
View SamplesThe purpose of this study was to determine whether postdevelopmental myostatin depletion influenced the changes in skeletal muscle gene expression profiles induced by a long-term increase in physical activity. Myostatin levels in muscles of adult male mice with floxed myostatin genes were reduced ~85% by activating Cre recombinase. Control mice with normal myostatin genes had the same Cre-activating treatment. Some of the mice were housed in ordinary cages throughout the study, limiting their physical activity. Other mice were given free access to running wheels for the final 12 weeks of the study. At the end of the study, comprehensive gene expression profiles of triceps brachii muscles were determined by RNA sequencing (RNA-Seq), with muscles from mice selected for similarity of running behavior throughout the period of wheel access. Wheel running increased expression of hundreds of mRNAs encoding proteins involved in oxidative energy metabolism, and this response was not affected by myostatin deficiency. The running-induced increase in the ratio of Myh1 mRNA (which encodes myosin heavy chain type 2x) to Myh4 mRNA (which encodes myosin heavy chain type 2b) also was not affected by myostatin depletion. At every threshold of P (computed by analysis of variance), the number of transcripts with interactions between activity level and myostatin level was fewer than the number expected by chance. These data suggest that myostatin is not required for transcriptional adaptations to moderate-intensity exercise. Overall design: 12 samples, 6 from sedentary mice and 6 from active (wheel running) mice. 3 control and 3 myostatin-deficient mice within each activity level.
Synergistic and antagonistic interplay between myostatin gene expression and physical activity levels on gene expression patterns in triceps Brachii muscles of C57/BL6 mice.
Specimen part, Subject
View SamplesThe immune system relies on the plasticity of its components to produce appropriate responses to frequent environmental challenges. Dendritic cells (DCs) are critical initiators of innate immunity and orchestrate the later and more specific adaptive immunity. The generation of diversity in transcriptional programs is central for effective immune responses. Alternative splicing is widely considered a key generator of transcriptional and proteomic complexity, but its role has been rarely addressed systematically in immune cells. Here we used splicing-sensitive arrays to assess genome-wide gene- and exon-level expression profiles in human DCs in response to a bacterial challenge. We find widespread alternative splicing events and splicing factor transcriptional signatures induced by an E. coli challenge to human DCs. Alternative splicing acts in concert with transcriptional modulation, but these two mechanisms of gene regulation affect primarily distinct functional gene groups. Alternative splicing is likely to have an important role in DC immunobiology because it affects genes known to be involved in DC development, endocytosis, antigen presentation and cell cycle arrest
Genome-wide analysis of alternative splicing during dendritic cell response to a bacterial challenge.
Specimen part, Treatment
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