8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, heart obtained at 12 weeks (thus animals were diabetic for 4 weeks). Left vent of heart.
Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart.
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View SamplesEffect of type 1 diabetes (induced by streptozotocin 60 mg/kg) on lung gene expression. Wistar rats, male. At age 8 weeks control rats got IP buffer, diabetic rats got streptozotocin. At age 12 weeks animals were anesthetized and lungs removed. RNA was extracted with Trizol, and gene expression array analysis was performed using Affymetrix RAE 230A microarrays according to the directions from the manufacturer. Arrays were scanned using a Hewlett Packard Gene Array scanner, and analyzed with Affymetrix MAS 5.0 software. Expression levels reported are the output from the MAS software.
Alterations in lung gene expression in streptozotocin-induced diabetic rats.
Age, Specimen part
View SamplesNormal young adult Sprague Dawley rats (male)
Differential expression of lipid and carbohydrate metabolism genes in upper airway versus diaphragm muscle.
No sample metadata fields
View SamplesComparison of gene expression of heart (left vent) and diaphragm of normal Sprague Dawley rats, young adult
Contrast between cardiac left ventricle and diaphragm muscle in expression of genes involved in carbohydrate and lipid metabolism.
No sample metadata fields
View Samples3 Cell lines from Apc, p53 (AP) GEMMs were compared to 12 cell lines from Apc, Kras, p53 (AKP) GEMMs.
Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation.
Sex, Cell line
View SamplesWe profiled global gene expression for two separate lines of mouse embryonic fibroblasts and find that deletion of PKM2 and expression of PKM1 does not alter global gene expression profiles.
Pyruvate kinase isoform expression alters nucleotide synthesis to impact cell proliferation.
No sample metadata fields
View SamplesThe human bone marrow (BM) gives rise to all distinct blood cell lineages, including CD1c+ and CD141+ myeloid dendritic cells (DC) and monocytes. These cell subsets are also present in peripheral blood (PB) and lymphoid tissues. However, the difference between the BM and PB compartment in terms of differentiation state and immunological role of DC is not yet known. The BM may represent both a site for development as well as a possible effector site and so far, little is known in this light with respect to different DC subsets. Using genome-wide transcriptional profiling we found clear differences between the BM and PB compartment and a location-dependent clustering for CD1c+ and CD141+ was demonstrated. DC subsets from BM clustered together and separate from the corresponding subsets from PB, which similarly formed a cluster. In BM, a common proliferating and immature differentiating state was observed for the two DC subsets, whereas DC from the PB showed a more immune-activated mature profile. In contrast, BM-derived slan+ non-classical monocytes were closely related to their PB counterparts and not to DC subsets, implying a homogenous prolife irrespective of anatomical localization. Additional functional tests confirmed these transcriptional findings. DC-like functions were prominently exhibited by PB DC. They surpassed BM DC in maturation capacity, cytokine production and induction of CD4+ and CD8+ T cell proliferation. This first study on myeloid DC in healthy human BM offers new information on steady-state DC biology and could potentially serve as a starting point for further research on these immune cells in healthy conditions as well as in diseases.
Human Bone Marrow-Derived Myeloid Dendritic Cells Show an Immature Transcriptional and Functional Profile Compared to Their Peripheral Blood Counterparts and Separate from Slan+ Non-Classical Monocytes.
Specimen part
View SamplesAbstract: Human 6-sulfo LacNac (slan)+ cells have been subject to a paradigm debate. They have previously been classified as a distinct dendritic cell (DC) subset. However, evidence has emerged that they may be more related to monocytes than to DC. To gain deeper insight into the functional specialization of slan+ cells, we have compared them with both conventional myeloid DC subsets (CD1c+ and CD141+) in human peripheral blood. Using genome-wide transcriptional profiling as well as extensive functional tests, we clearly show that slan+ cells form a distinct, non-DC-like, population. They cluster away from both DC subsets and their gene expression profile evidently suggests involvement in distinct inflammatory processes. An extensive comparison with existing genomic data sets also strongly confirmed the relationship of slan+ with the monocytic compartment rather than with DC. From a functional perspective, their ability to induce CD4+ and CD8+ T cell proliferation is relatively low. Combined with the finding that antigen presentation by MHC class II is at the top of under-represented pathways in slan+ cells, this points to a minimal role in directing adaptive T cell immunity. Rather, the higher expression of complement receptors on their cell surface, together with their high secretion of IL-1 and IL-6, imply a specific role in innate inflammatory processes, which is consistent with their recent identification as non-classical monocytes. This study extends our knowledge on DC/monocyte subset biology under steady state conditions and contributes to our understanding of their role in immune-mediated diseases and their potential use in immunotherapeutic strategies.
Transcriptional profiling reveals functional dichotomy between human slan<sup>+</sup> non-classical monocytes and myeloid dendritic cells.
Specimen part
View SamplesGlobal transcriptome patterns were obtained from ATAF1-IOE seedlings at 1 h, 2 h and 5 h after estradiol induction or mock treatment, and from mature ATAF1-IOE leaves at 5 h after estradiol induction or mock treatment.
Transcription Factor Arabidopsis Activating Factor1 Integrates Carbon Starvation Responses with Trehalose Metabolism.
Specimen part, Treatment, Time
View SamplesMutations in the gene encoding the transcription factor AutoImmune REgulator (AIRE) are responsible for the Autoimmune PolyEndocrinopathy Candidiasis Ecodermal Dystrophy syndrome. AIRE directs expression of tissue restricted antigens in the thymic medulla and in lymph node stromal cells and thereby substantially contributes to induction of immunological tolerance to self-antigens. Data from experimental mouse models showed that AIRE-deficiency leads to impaired deletion of autospecific T cell precursors. However, a potential role for AIRE in the function of regulatory T cell populations, which are known to play a central role in prevention of immunopathology, has remained elusive. Regulatory T cells of CD8+CD28low phenotype efficiently control immune responses in experimental autoimmune and colitis models in mice. We here show that CD8+CD28low Treg from AIRE-deficient mice are transcriptionally and phenotypically normal, exert efficient suppression of in vitro immune responses, but completely fail to prevent experimental colitis in vivo. Our data therefore demonstrate that AIRE plays an important role in the in vivo function of a naturally occurring regulatory T cell population.
Autoimmune regulator (AIRE)-deficient CD8+CD28low regulatory T lymphocytes fail to control experimental colitis.
Treatment
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