Transcription profiling of human hematopoietic stem/progenitor cells treated with TGF-beta1 to idetntify its target genes
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ABSTRACT: CD34+ hematopoietic stem/progenitor cells were isolated from human cord blood and amplified in vitro for 10-14 days in serum-free medium with specific cytokines (Ju et al., Eur. J. Cell Biol. 82, 75-86, 2003; Hacker et al., Nat. Immunol. 4, 380-386, 2003). Cells were then treated with TGF-beta1 for various periods of time (2, 4, 16 hours) and RNA was prepared and subjected to microarray analysis. Experiment Overall Design: CD34+ hematopoietic stem/progenitor cells (HPC) were amplified in vitro and treated with TGF-beta1 (10 ng/ml) for 2, 4 and 16 hours. Experiment Overall Design: HPC untreated Experiment Overall Design: HPC + TGF-beta1 for 2 hours Experiment Overall Design: HPC + TGF-beta1 for 4 hours Experiment Overall Design: HPC + TGF-beta1 for 16 hours
Project description:This SuperSeries is composed of the following subset Series:; GSE5150: TGF-beta1 target genes in human hematopoietic stem/progenitor cells. GSE5151: TGF-beta1 target genes in human dendritic cells (DC). Experiment Overall Design: Refer to individual Series
Project description:CD34+ hematopoietic stem/progenitor cells were isolated from human cord blood and amplified in vitro for 10-14 days in serum-free medium with specific cytokines (Ju et al., Eur. J. Cell Biol. 82, 75-86, 2003; Hacker et al., Nat. Immunol. 4, 380-386, 2003). Cultured progenitor cells were induced to differentiate into DC in RPMI medium supplemented with 10% fetal calf serum, 2 mM L-glutamine, 0.1 microM Beta-mercaptoethanol, 100 U/ml penicillin and streptomycin (GIBCO-BRL) and 500 U/ml GM-CSF, 500 U/ml IL-4 for 6 days with or without 10 ng/ml TGF-beta1 as indicated (0.5x10E6 cells/ml). Every 2 days growth factors were added and cells were maintained at 0.5x10E6 cells/ml cell density. RNA was prepared and subjected to microarray analysis. Experiment Overall Design: Dendritic cells (DC) were treated for various periods of time (4, 16 and 36 hours) with TGF-beta1 (10 ng/ml) or left untreated. Experiment Overall Design: DC untreated Experiment Overall Design: DC + TGF-beta1 for 4 hours Experiment Overall Design: DC + TGF-beta1 for 16 hours Experiment Overall Design: DC + TGF-beta1 for 36 hours
Project description:This SuperSeries is composed of the following subset Series: GSE38133: TGF-beta1 effect on human osteosarcoma cell line MNNG/HOS GSE38134: Expression analysis of human osteosarcoma cell line MNNG/HOS sarcospheres, hypoxia-induced sarcospheres and TGF-beta1-induced sarcospheres Refer to individual Series
Project description:Gene expression profiling of a total of 3,774 genes in primary osteoblastic cells treated with TGF-beta1 Keywords: cytokine response Primary osteoblasts cultured under serum-starved condition were treated or untreated with TGF-beta1 for 24 hr.
Project description:Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). Total RNA was prepared from unstimulated cells (Pre-TGF) of similar passage and compared by microarray analysis. The two groups were analyzed in triplicate, three Pre-TGF samples and three Post-TGF-Rec samples.
Project description:Invastigation of whole genome gene expression level changes in human osteosarcoma cell line MNNG/HOS sarcospheres,hypoxia-induced sarcospheres and TGF-beta1 induced sarcospheres. A three chip study using total RNA cover from three cultures of human osteosarcoma cell line MNNG/HOS sarcospheres, hypoxia-induced sarcospheres and TGF-beta1-induced sarcospheres. Each chip measures the expression level of 45033 genes from osteosarcoma cell line MNNG/HOS.
Project description:TGF-beta3 produced by developing Th17 cells induces highly pathogenic T cells that are functionally and molecularly distinct from TGF-beta1-induced Th17 cells. The microarray data represent a distinct molecular signature for pathogenic versus non-pathogenic Th17 cells. Total of seven groups with two to four samples per group from two independent experiments. The no cytokines group (Th0) was used as a control to normalize the data. 7 groups: B6: (IL-1beta, IL-6) B623: (IL-1beta, IL-6, IL-23) T16: (TGF-beta1, IL-6) T1623: (TGF-beta1, IL-6, IL-23) T36: (TGF-beta3, IL-6) T3623: (TGF-beta3, IL-6, IL-23) NOCYTO: no cytokines
Project description:Investigation of whole genome gene expression level changes in human osteosarcoma cell line MNNG/HOS treated by TGF-beta1 for three days (mesophase) and five days (sarcospheres iOSCs), compared to non-treatment cells (residual adherent cells). A three chip study using total RNA cover from three cultures of non-treatment human osteosarcoma cell line MNNG/HOS (residual adherent cells), TGF-beta1 treated three days osteosarcoma cell line MNNG/HOS (mesophase) and TGF-beta1 treated five days osteosarcoma cell line MNNG/HOS ( only collected the suspending sarcospheres iOSCs). Each chip measures the expression level of 45033 genes from osteosarcoma cell line MNNG/HOS.
Project description:Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study different murine hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro-proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell-type-specific proliferation. First, cell-type-specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate-limiting for faster-cycling cells while slower cell-cycles are controlled at the G1-S progression. The integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and faithfully predicts based on the protein abundance anti-proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance patterns.