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GSE15569
Homo sapiens
6 Downloadable Samples
Illumina HumanWG-6 v3.0 expression beadchip
Description
Several studies indicate that adult stem cells may improve the recovery from acute tissue injury. It has been suggested that they may contribute to tissue regeneration by the release of paracrine factors promoting proliferation of tissue resident cells. However, the factors involved remain unknown. In the present study we found that microvesicles (MV) derived from human liver stem cells (HLSC) were able to stimulate in vitro proliferation and apoptosis resistance of human and rat hepatocytes. These effects required internalization of MV in the hepatocytes by an alpha4 integrin-dependent mechanism. However, when treated with RNase, MV despites their internalization were unable to induce hepatocyte proliferation and apoptosis resistance, suggesting an RNA dependent effect. Microarray analysis and quantitative RT-PCR demonstrated that MV were shuttling a specific subset of cellular mRNA, such as mRNA associated in the control of transcription, translation, proliferation and apoptosis. When administered in vivo, MV were found to accelerate the morphological and functional recovery of liver in a model of 70% hepatectomy in rats by inducing an hepatocytes proliferation that was abolished by RNase treatment. Using human AGO2 gene, which is shuttled by MV, as a reporter gene, we found the expression of human AGO2 mRNA and protein in the liver of hepatectomized rats treated with MV. This suggest a translation of the MV shuttled mRNA within hepatocytes of treated rats. Conclusion: these results suggest that MV derived from HLSC may activate a proliferative program in remnant hepatocytes after hepatectomy by a horizontal transfer of specific mRNA subsets.
Publication Title
Human liver stem cell-derived microvesicles accelerate hepatic regeneration in hepatectomized rats.
Sample Metadata Fields
Specimen part
View Samples- Oryza sativa
- 44 Downloadable Samples
- Affymetrix Rice (US) Gene 1.0 ST Array (rusgene11st)
Description
The approval of genetically modified (GM) crops is preceded by years of intensive research to demonstrate safety to humans and environment. We recently showed that in vitro culture stress is the major factor influencing proteomic differences of GM vs. non-GM plants. This made us question the number of generations needed to erase such memory. We also wondered about the relevance of alterations promoted by transgenesis as compared to environment-induced ones.
Publication Title
Environmental stress is the major cause of transcriptomic and proteomic changes in GM and non-GM plants.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 33 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Molecular pathways activated in MALT lymphoma are not well defined.
Publication Title
Gene expression profiling of pulmonary mucosa-associated lymphoid tissue lymphoma identifies new biologic insights with potential diagnostic and therapeutic applications.
Sample Metadata Fields
Sex
View Samples- Arabidopsis thaliana
- 22 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Identification of TBF1-dependent and SA, elf18-responsive genes in Arabidopsis
Publication Title
The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Caenorhabditis elegans
- 15 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
C. elegans exhibit an age-dependent mechanical stress response to blunt force injury.
Publication Title
Trauma-induced regulation of VHP-1 modulates the cellular response to mechanical stress.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
Illumina HiSeq 2000
Description
We report here that REV-ERBa influences nuclear localization of the glucocorticoid receptor and vice versa. As a consequence these two nuclear receptors influence each others transcriptome. REV-ERBa (Nr1d1) is a nuclear receptor that is part of the circadian clock mechanism and regulates metabolism and inflammatory processes. The glucocorticoid receptor (GR, Nr3c1) influences similar processes, but is not part of the circadian clock mechanism although glucocorticoid signaling affects resetting of the circadian clock in peripheral tissues. Because of their similar impact on physiological processes we studied the interplay between these two nuclear receptors. We found that REV-ERBa competes with GR for binding to HSP90, a chaperone responsible for the activation of substrate proteins to ensure survival of a cell. This competition affected stability and nuclear localization of GR, thereby affecting GR target gene expression such as I?B and alcohol dehydrogenase 1 (Adh1). Our findings highlight an important interplay between two nuclear receptors that influence each others transcritpional potential indicating that the transcriptional landscape is strongly dependent on dynamic processes at the protein level. Overall design: In this dataset, we isolated livers at Zeitgebertime (ZT) 8 and ZT20 of wild type and Rev-erb alpha knock-out animals. Liver samples were immediately flash frozen in liquid N2 and stored at -80?°C. RNA was extracted using NucleoSpin RNA (Machery-Nagel, Düren, Germany) according to the instructions of the manufacturer. Quality of the RNA samples was analysed with a spectrophotometer, agarose gel electrophoresis and reverse transcription-PCR. Library construction starting from the poly(A)-tail and multiplexing was performed according to the instructions of the manufacturer (Illumina). The samples were organized as follows: Three replicas (1-WT, 2-WT, 3-WT) correspond to genotype WT at ZT8. Three replicas (4-Rev, 5-Rev, 6-Rev) correspond to genotype Rev-/- at ZT8. Three replicas (7-WT, 8-WT, 9-WT) correspond to genotype WT at ZT20. Three replicas (10-Rev, 11-Rev, 12-Rev) correspond to genotypeRev-/- at ZT20. For the experiment, complementary DNA (cDNA) libraries were barcoded using Illumina primers and loaded onto one lane of an IlluminaHS2000 machine. cDNA libraries were diluted and loaded onto each lane. The samples were sequenced for a maximum sequencing length of 75?bp. Sequences were aligned to the mouse genome (UCSC version mm10 database). Numbers of the sequences obtained for each library can be found in Supplementary Table 3. Sequences (fastq format) were mapped with Tophat (Trapnell, C. 2009), uniquely mapped sequences from the output files (bam format) were then used for further analysis, percentage of the mapping obtained for each sample can be found in Supplementary Table 3. For all files the reads were counted with HTSeq-count using the following criteria: samtools view sample.bam | htseq-count -m union -a 10 -s no -i gene_name Mus_Musculus.gtf > sample_counts.txt Tests for differential expression between the samples were performed in R software (R Core Team, 2014 http://www.R-project.org/) using the DESeq2 package (Version 1.6.3) (Love, M. 2014). A threshold on the corrected P value was used to call for differentially expressed genes (P.adjust<0.05).
Publication Title
REV-ERBα influences the stability and nuclear localization of the glucocorticoid receptor.
Sample Metadata Fields
Age, Specimen part, Subject, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2500
Description
BACKGROUND: Combination antiretroviral therapy (cART) is able to control HIV-1 viral replication, however long-lived latent infection in resting memory CD4+ T-cells persist. The mechanisms for establishment and maintenance of latent infection in resting memory CD4+ T-cells remain unclear. Previously we have shown that HIV-1 infection of resting CD4+ T-cells co-cultured with CD11c+ myeloid dendritic cells (mDC) produced a population of non-proliferating T-cells with latent infection. Here we asked whether different antigen presenting cells (APC), including subpopulations of DC and monocytes, were able to induce post-integration latent infection in resting CD4+ T-cells, and examined potential cell interactions that may be involved using RNA-seq. RESULTS: mDC (CD1c+), SLAN+ DC and CD14+ monocytes were most efficient in stimulating proliferation of CD4+ T-cells during syngeneic culture and in generating post-integration latent infection in non-proliferating CD4+ T-cells following HIV-1 infection of APC-T-cell co-cultures. In comparison, plasmacytoid DC (pDC) and B-cells did not induce latent infection in APC-T-cell co-cultures. We compared the RNA expression profiles of APC subpopulations that could and could not induce latency in non-proliferating CD4+ T-cells. Gene expression analysis, comparing the mDC, SLAN+ DC and CD14+ monocyte subpopulations to pDC identified 53 upregulated genes that encode proteins expressed on the plasma membrane that could signal to CD4+ T-cells via cell-cell interactions (32 genes), immune checkpoints (IC) (5 genes), T-cell activation (9 genes), regulation of apoptosis (5 genes), antigen presentation (1 gene) and through unknown ligands (1 gene). CONCLUSIONS: APC subpopulations from the myeloid lineage, specifically mDC subpopulations and CD14+ monocytes, were able to efficiently induce post-integration HIV-1 latency in non-proliferating CD4+ T-cells in vitro. Inhibition of key pathways involved in mDC-T-cell interactions and HIV-1 latency may provide novel targets to eliminate HIV latency. Overall design: mRNA profiles of sorted, pure antigen presenting cells including, CD1c+ myleoid dendirtic cells (mDC), SLAN+ mDC, CD14+ monocytes and plasmacytoid DC (pDC), were generated using next generation sequencing in triplicate, using Illumina Illumina Hiseq 2000.
Publication Title
The role of antigen presenting cells in the induction of HIV-1 latency in resting CD4(+) T-cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500, Illumina HiSeq 2000
Description
Relatively little is known about how the identity of early neuronal stem cells changes before and after neural tube closure (neurulation). We performed RNA sequencing on microdissected forebrain precursors and revealed sharp reductions in expresion of protein biosynthetic machinery after neurulation. These reductions were paralleled by down-regulation of Myc, which regulated forebrain precursor ribosome ribosome biogenesis. To study consequences of Myc dysregulation, we overexpressed Myc in Nestin+ neural progenitors, sorted these progenitors for RNA sequencing, and identified 135 genes that are differentially expressed between Myc-overexpressed embryos and their wildtype littermates. Overall design: The first RNA sequencing dataset contains micordissected neuroepithelium from E8.5 and E10.5 mouse embryos, two biological replicates for each age. The second RNA sequencing dataset contain FACS isolated Pax6+ neural progenitors form the cortex of E13.5 MYC-overexpressed embryos and their wildtype littermates, three biological replicates for each genotype.
Publication Title
Downregulation of ribosome biogenesis during early forebrain development.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 31 Downloadable Samples
- Illumina HiSeq 2500
Description
C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, is primarily expressed on cells of the myeloid lineage, and to a lesser extent on endothelial cells and neurons in brain. Previous work demonstrated C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive deficits in Alzheimer Disease (AD) mouse models. In the Arctic AD mouse model, genetic deletion of C5aR1 prevented behavior deficits at 10 months. However, the molecular mechanisms of this protection has not been definitively demonstrated. To understand the role of microglial C5aR1 in the Arctic AD mouse model, we have taken advantage of the CX3CR1GFP and CCR2RFP reporter mice to distinguish microglia as GFP-positive and infiltrating monocytes as GFP and RFP positive, for subsequent transcriptome analysis on specifically sorted myeloid populations from wild type and AD mouse models. Immunohistochemical analysis of mice aged to 2, 5, 7 and 10 months showed no change in amyloid beta (Ab) deposition in the Arctic C5aR1 knockout (KO) mice relative to that seen in the Arctic mice. Of importance, no CCR2+ monocytes/macrophages were found near the plaques in the Arctic brain with or without C5aR1. RNA-seq analysis on microglia from these mice identified inflammation related genes as differentially expressed, with increased expression in the Arctic mice relative to wildtype and decreased expression in the Arctic/C5aR1KO relative to Arctic. In addition, phagosomal-lysosomal proteins and protein degradation pathways that were increased in the Arctic mice were further increased in the Arctic/C5aR1KO mice. These data are consistent with a microglial polarization state with restricted induction of inflammatory genes and enhancement of clearance pathways. Overall design: Microglia mRNA profiles of wildtype (WT), C5aR1 knockout (C5aR1KO), Arctic (ARC) and Arctic C5aR1 knockout (ARCKO) mice at 2, 5, 7 and 10-11 month. Duplicates were sequenced for each genotype on Illumina HiSeq 2500 platform.
Publication Title
Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Homo sapiens
- 45 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Detection of specific chromosomal abnormalities by FISH and metaphase cytogenetics allows risk stratification in multiple myeloma (MM); however, gene expression profiling (GEP) based signatures may enable more specific risk categorization.
Publication Title
Impact of gene expression profiling-based risk stratification in patients with myeloma receiving initial therapy with lenalidomide and dexamethasone.
Sample Metadata Fields
Specimen part, Disease
View Samples