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GSE6055
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
The murine model of Lyme disease provides a unique opportunity to study the localized host response to similar stimulus, B. burgdorferi, in the joints of mice destined to develop severe arthritis (C3H) or mild disease (C57BL/6). Pathways associated with the response to infection and the development of Lyme arthritis were identified by global gene expression patterns using oligonucleotide microarrays. A robust induction of IFN responsive genes was observed in severely arthritic C3H mice at one week of infection, which was absent from mildly arthritic C57BL/6 mice. In contrast, infected C57BL/6 mice displayed a novel expression profile characterized by genes involved in epidermal differentiation and wound repair, which were decreased in the joints of C3H mice. These expression patterns were associated with disease state rather than inherent differences between C3H and C57BL/6 mice, as C57BL/6-IL10-/- mice infected with B. burgdorferi develop more severe arthritis that C57BL/6 mice and displayed an early gene expression profile similar to C3H mice. Gene expression profiles at two and four weeks post infection revealed a common response of all strains that was likely to be important for the host defense to B. burgdorferi and mediated by NF-kB-dependent signaling. The gene expression profiles identified in this study add to the current understanding of the host response to B. burgdorferi and identify two novel pathways that may be involved in regulating the severity of Lyme arthritis.
Publication Title
Gene expression profiling reveals unique pathways associated with differential severity of lyme arthritis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Mesenchymal stromal cells (MSC) were isolated from human bone marrow. Here, we have compared gene expression profiles of MSC at early and late passages and upon stimulation with transforming growth factor beta 1 (TGF-b1). Stimulation was performed with 1ng/mL TGF-b1 for 1, 4, or 12 hours as indicated. The goal of this study was to determine if senescence-associated gene expression changes and TGF-b1 induced gene expression changes are related.
Publication Title
TGF-beta1 does not induce senescence of multipotent mesenchymal stromal cells and has similar effects in early and late passages.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Multipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Ser et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
We here compared gene expression profiles in HepG2 cells upon stimulation with 1 ng/ml TGF-beta1 for 20 min, 1 hour, 2 hours, 4 hours, and 24 hours with untreated control cells. Experiments were done in three independent replicates. The goal of this study was to determine genes regulated by TGF-beta1.HepG2 cells were obtained from DSMZ (Braunschweig, Germany) and cell identity confirmed by STR profiling using the AmpFlSTR Identfiler Direct PCR Amplification kit (Life Technologies, Darmstadt, Germany). Gene expression profiles were compared at indicated time points after stimulation with TGF-beta (1 ng/ml) using the Human Gene 1.0 ST arrays (Affymetrix). In total 18 hybridizations are included in this series.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We here compared gene expression profiles of primary murine hepatocytes (mPC) upon stimulation with 1 ng/ml TGF-beta1 for 20 min, 2 hours and 4 hours with untreated cells. Experiments were done in three independent replicates. The goal of this study was to determine genes regulated by TGF-beta1.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Mus musculus
- 11 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury and cancer. Deletion of NF-B essential modulator in hepatocytes (Nemohepa) causes the spontaneous development of hepatocellular carcinoma preceded by steatohepatitis in mice and thus serves as an excellent model for the progression from chronic hepatitis to liver cancer. In the present study we aimed to dissect the death-receptor mediated pathways that contribute to liver injury in Nemohepa mice. Therefore, we generated Nemohepa/TRAIL-/- and Nemohepa/TNFR1-/- animals and analyzed the progression of liver injury. Nemohepa/TRAIL-/- displayed a similar phenotype to Nemohepa mice characteristic of high apoptosis, infiltration of immune cells, hepatocyte proliferation and steatohepatitis. These pathophysiological features were significantly ameliorated in Nemohepa/TNFR1-/- livers. Hepatocyte apoptosis was increased in Nemohepa and Nemohepa/TRAIL-/- mice while Nemohepa/TNFR1-/- animals showed reduced cell death concomitant with a strong reduction in pJNK levels. Cell cycle parameters were significantly less activated in Nemohepa/TNFR1-/- livers. Additionally, markers of liver fibrosis and indicators of tumour progression were significantly decreased in these animals. The present data demonstrate that the death receptor TNFR1 but not TRAIL is important in determining progression of liver injury in hepatocyte-specific Nemo knockout mice.
Publication Title
TNFR1 determines progression of chronic liver injury in the IKKγ/Nemo genetic model.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gene expression profile of joint tissue from C3H and interval specific congenic mouse lines (ISCL) following infection with Borrelia burgdorferi
Publication Title
Interval-specific congenic lines reveal quantitative trait Loci with penetrant lyme arthritis phenotypes on chromosomes 5, 11, and 12.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 3 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
The colorectal cancer (CRC) cell line pair SW480/SW620 is an accepted model to study CRC progression and metastasis formation. Studying gene expression differences might allow to uncover molecular mechanisms that underlie metastasis initiation
Publication Title
The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 23 Downloadable Samples
Illumina HiSeq 2000
Description
T lymphocytes are essential contributors to the adaptive immune system and consist of multiple lineages that serve various effector and regulatory roles. As such, precise control of gene expression is essential to the proper development and function of these cells. Previously, we identified Snai2 and Snai3 as being essential regulators of immune tolerance partly due to the impaired function of CD4+ regulatory T cells in Snai2/3 conditional double knockout mice. Here we extend those previous findings using a bone marrow transplantation model to provide an environmentally unbiased view of the molecular changes imparted onto various T lymphocyte populations once Snai2 and Snai3 are deleted. The data presented here demonstrate that Snai2 and Snai3 transcriptionally regulate the cellular fitness and functionality of not only CD4+ regulatory T cells but effector CD8a+ and CD4+ conventional T cells as well. This is achieved through the modulation of gene sets unique to each cell type and includes transcriptional targets relevant to the survival and function of each T cell lineage. As such, Snai2 and Snai3 are essential regulators of T cell immunobiology. Overall design: GFP- CD3e+ CD8a+ CD4-, GFP- CD3e+ CD8a- CD4+ CD25- and GFP- CD3e+ CD8a- CD4+ CD25+ T cells were isolated from spleens of UBC-GFP mice transplanted with WT or cDKO lineage-depleted donor bone marrow following lethal irradiation of recipient mice. RNA-seq was performed on 3-4 biological replicates from each genotype for all T cell populations analyzed.
Publication Title
Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples