Effector CD8+ T cells are believed to be terminally differentiated cells having cytotoxic activity and the ability to produce effector cytokines such as INF- and TNF-. We investigated the difference between CXCR1+ and CXCR1- subsets of human effector CD27-CD28-CD8+ T cells. Both subsets similarly expressed cytolytic molecules and exerted substantial cytolytic activity, whereas only the CXCR1- subset had IL-2 productivity and self-proliferative activity and was more resistant to cell death than the CXCR1+ subset. These differences were explained by the specific up-regulation of CAMK4, SPRY2, and IL-7R in the CXCR1- subset and that of pro-apoptotic DAPK1 in the CXCR1+ subset. The IL-2 producers were more frequently found in the IL-7R+ subset of the CXCR1- effector CD8+ T cells than in the IL-7R- subset. IL-7/IL-7R signaling promoted cell survival only in the CXCR1- subset. The present study has highlighted a novel subset of effector CD8+ T cells producing IL-2 and suggests the importance of this subset in the homeostasis of effector CD8+ T cells.
Functional heterogeneity of human effector CD8+ T cells.
Sex, Specimen part
View SamplesTo understand the molecular mechanism by which regulate skeletal development, we attempted to identify transcription factors that were highly expressed in developing cartilage during the embryonic stage.
The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification.
Specimen part
View SamplesThe early blood vessels of the embryo and yolk sac in mammals develop by aggregation of de novo forming angioblasts into a primitive vascular plexus, which then undergoes a complex remodeling process. Angiogenesis is also important for disease progression in the adult. However, the precise molecular mechanism of vascular development remains unclear.
Genome-wide identification of endothelial cell-enriched genes in the mouse embryo.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.
Specimen part, Cell line, Treatment
View SamplesProstate cancer is the most common cancer in men. We identified that miR-29 family is the most androgen-responsive miRNA in hormone-refractory prostate cancer cells. For the screening of miR-29b target, we performed microarray analysis in two prostate cancer cells. Because TET2 is the primary target of miR-29 family by our analysis, we also performed TET2 signaling by microarray.
TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.
Specimen part, Cell line
View SamplesWe performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold.
Identification of genetic networks involved in the cell growth arrest and differentiation of a rat astrocyte cell line RCG-12.
No sample metadata fields
View SamplesTo detect transcripts before and after APH treatment, we subjected total RNA isolated from U2OS cells expressing human FANCD2-3xFLAG to next generation sequencing. Overall design: U2OS cells expressing human FANCD2-3xFLAG were treated with 0.4 micro M APH, or left antreated for 24 hrs.
Replication stress induces accumulation of FANCD2 at central region of large fragile genes.
Treatment, Subject
View SamplesWe performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation.
Establishment and functional characterization of a tracheal epithelial cell line RTEC11 from transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen.
No sample metadata fields
View SamplesDiet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor antagonist and a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, reportedly has beneficial effects on insulin sensitivity. We studied the effects of telmisartan on the adipose tissue macrophage phenotype in high fat-fed mice. Telmisartan was administered for 5 weeks to high fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in epididymal fat tissues were examined. Insulin- or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight and adipocyte size without affecting the amount of food intake. Telmisartan treatment reduced the number of CD11c-positive cells and crown-like structures. Telmisartan reduced the mRNA expressions of M1 macrophage markers, such as TNF-alpha and IL-6, and increased the expression of M2 markers, such as IL-10 and Mgl2. The reduction of M1 macrophage markers, as well as the increased gene expression of M2 markers especially IL-10, is a possible mechanism for the improvement of insulin sensitivity by telmisartan.
Telmisartan improves insulin resistance and modulates adipose tissue macrophage polarization in high-fat-fed mice.
Sex, Specimen part, Treatment
View SamplesThe liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secreted proteins, termed hepatokines.
A liver-derived secretory protein, selenoprotein P, causes insulin resistance.
Sex, Specimen part, Disease
View Samples