Background: Preterm birth is the leading cause of all infant mortality. In 2004, 12.5% of all births were preterm. In order to understand preterm labor, we must first understand normal labor. Since many of the myometrial changes that occur during pregnancy are similar in mice and humans and mouse gestation is short, we have studied the uterine genes that change in the mouse during pregnancy. Here, we used microarray analysis to identify uterine genes in the gravid mouse that are differentially regulated in the cyclooxygenase-1 knockout mouse model of delayed parturition.
Identification of 9 uterine genes that are regulated during mouse pregnancy and exhibit abnormal levels in the cyclooxygenase-1 knockout mouse.
No sample metadata fields
View SamplesThrough RNA sequencing and gene ontology analyses, we report that immune activation is elicited in the spleen of 4 HIV-1-infected humanized mice when compared to 4 mock-infected humanized mice. Overall design: mRNA expression profiles in the splenic human mononuclear cells of HIV-1-infected humanized mice at 6 weeks post-infection (n=4) and mock-infected humanized mice (n=4) were generated by RNA sequencing. RNA was extracted using QIAamp RNA Blood Mini kit (Qiagen). RNA sequencing was conducted in Medical & Biological Laboratories, co (Nagoya, Japan).
HIV-1 competition experiments in humanized mice show that APOBEC3H imposes selective pressure and promotes virus adaptation.
Specimen part, Subject, Time
View SamplesComparative transcriptomic analysis of Arabidopsis thaliana yda11 plants (in Col-0 background), and wild-type plants (Col-0) non-infected or infected with the necrotrophic fungal pathogen Plectosphaerella cucumerina BMM (PcBMM)
YODA MAP3K kinase regulates plant immune responses conferring broad-spectrum disease resistance.
Specimen part, Treatment, Time
View SamplesWe compared gene expression profiles of a human CD4+ T-cell line 24 h after infection with a cell line of the same origin permanently releasing SIVmac251/32H. A new knowledge-based-network approach (Inter-Chain-Finder) was used to identify subnetworks leading to resistance to SIV-induced cell death. Notably, the method can identify not only differentially-expressed key hub genes but also non-differentially expressed, critical, hidden regulators.
Identification of molecular sub-networks associated with cell survival in a chronically SIVmac-infected human CD4+ T cell line.
Disease, Disease stage
View SamplesSilicosis, a fibrotic granulomatous lung disease, may occur through accidental high-dose or occupational inhalation of silica, leading to acute/accelerated and chronic silicosis, respectively. While chronic silicosis has a long asymptomatic latency, lung inflammation and apoptosis are hallmarks of acute silicosis. In animal models, histiocytic granulomas develop within days after high-dose intratracheal silica instillation. However, following chronic inhalation of occupationally relevant doses of silica, discrete granulomas resembling human silicosis arise months after the final exposure without significant lung inflammation/apoptosis. To identify molecular events associated with chronic silicosis, lung RNAs from controls or chronically silica-exposed rats were analyzed by Affymetrix at 28 wk after silica exposures. Results suggested a significant upregulation of 144 genes and downregulation of seven genes. The upregulated genes included complement cascade, chemokines/chemokine receptors, G-protein signaling components, metalloproteases, and genes associated with oxidative stress. To examine the kinetics of gene expression relevant to silicosis, qPCR, ELISA, Luminex-bead assays, Western blotting, and/or zymography were performed on lung tissues from 4 d, 28 wk, and intermediate times after chronic silica exposure and compared with 14 d acute silicosis samples. Results indicated that genes regulating fibrosis (secreted phosphoprotein-1, CCL2, and CCL7), redox enzymes (superoxide dismutase-2 and arginase-1), and the enzymatic activities of matrix metalloproteinases 2 and 9 were upregulated in acute and chronic silicosis; however, proinflammatory cytokines were strongly upregulated only in acute silicosis. Thus, inflammatory cytokines are associated with acute but not chronic silicosis; however, genes regulating fibrosis, oxidative stress, and metalloproteases may contribute to both acute and chronic silicosis.
Fibrogenic and redox-related but not proinflammatory genes are upregulated in Lewis rat model of chronic silicosis.
Specimen part, Treatment
View SamplesAnalysis of the transcriptomes of nearly ripe siliques (18-19 DAP) of the rdo2-1, rdo3 and hub1-2 (rdo4) mutants in comparison with wild-type Ler, using Affymetrix GeneChip Arabidopsis ATH1 Genome Array.
Identification of the Arabidopsis REDUCED DORMANCY 2 gene uncovers a role for the polymerase associated factor 1 complex in seed dormancy.
No sample metadata fields
View SamplesAnalysis of the transcriptome of dry hda9-1 mutant seeds with those of Col wild-type seeds, using Affymetrix GeneChip Arabidopsis ATH1 Genome Array.
HISTONE DEACETYLASE 9 represses seedling traits in Arabidopsis thaliana dry seeds.
Specimen part
View SamplesCo-treatment with soluble CD74 and MIF induced necroptosis in cardiac myofibroblasts. The underlying mechanism of sCD74/MIF-induced necroptosis are still unkown. We used a microarray to identify pathways regulated by co-treatment with sCD74 and MIF .
Soluble CD74 Reroutes MIF/CXCR4/AKT-Mediated Survival of Cardiac Myofibroblasts to Necroptosis.
Specimen part
View SamplesIKB Kinase beta (IKKB), a key component of the NFKB signalling pathway plays an important role in inflammation and cancer. Here we describe a previously unknown role of the IKK/FoxO3a axis in bone metastasis. We found that IKK was highly expressed in invasive human breast tumours and that levels of expression were elevated in bone metastasis. Overexpression of IKK in parental and bone-tropic human breast cancer cell-lines increased tumour volume, worsened cachexia, promoted osteolysis and increased mortality in adult mice whereas pharmacological inhibition and knockdown of IKK were inhibitory. Inhibition of IKK in breast cancer cell lines and bone cells stimulated bone formation and reduced tumour growth by a mechanism that was mediated in part, by cytoplasmic sequestering of FoxO3a independently of NFKB inhibition. We conclude that IK contributes significantly to the regulation of tumour growth and osteolysis in breast cancer by NFKB dependent and independent mechanisms.
Regulation of breast cancer induced bone disease by cancer-specific IKKβ.
Cell line
View SamplesIntravesical BCG Immunotherapy is the standard of care in treating non-muscle invasive bladder cancer, yet its mechanism of action remains elusive. Both innate and adaptive immune responses have been implicated in BCG activity. While prior research has indirectly demonstrated the importance of T cells and shown a rise in CD4+ T cells in bladder tissue after BCG, T cell subpopulations have not been fully characterized. We investigated the relationship between effector and regulatory T cells in an immune competent, clinically relevant rodent model of bladder cancer. Our data demonstrate that cancer progression in the MNU rat model of bladder cancer is characterized by a decline in the CD8/FoxP3 ratio, consistent with decreased adaptive immunity. By contrast, treatment with intravesical BCG leads to a large, transient rise in the CD4+ T cell population in the urothelium, and is both more effective and immunogenic compared to intravesical chemotherapy. Interestingly, whole transcriptome expression profiling of post-treatment intravesical CD4+ and CD8+ T cells revealed minimal differences in gene expression after BCG treatment. Together, our results suggest that while BCG induces T cell recruitment to the bladder, the T cell phenotype does not markedly change, implying that combining T cell activating agents with BCG might improve clinical activity.
Intravesical BCG Induces CD4<sup>+</sup> T-Cell Expansion in an Immune Competent Model of Bladder Cancer.
Specimen part, Treatment
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