Adenosine-treated endothelial progenitor cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE26744 | GEO | 2011/01/29
SECONDARY ACCESSION(S): PRJNA136331
REPOSITORIES: GEO
Similar Datasets
Project description:The goal of this study was to investigate the effects of the cardioprotective nucleoside adenosine on gene expression in early and late endothelial progenitor cells. Adenosine mod Early outgrowth endothelial progenitor cells were obtained by adhesion of peripheral blood mononuclear cells of healthy volunteers. Late endothelial progenitor cells were obtained by purification of CD34+ peripheral blood cells and were cultured and amplified in endothelial-specific medium containing growth factors. Both cell types were treated by adenosine (10micromol/L) for 6 hours. Total RNA was extracted using conventional Trizol extraction, quantified by Nanodrop and analyzed by Bioanalyzer. 1microg of RNA was amplified using AminoAllyl MessageAmp kit. 5µg amino allyl-coupled RNA was labeled with Cy3 or Cy5 dyes. Dye coupling yield >5% was a prerequisite for further analysis. 750ng of labeled RNA was hybridized on 25,000 gene microarrays for 17 hours at 60°C. 4 arrays per sample were hybridized and scanned with the Genepix 4000B Scanner (Molecular Devices). Six independent experiments were performed. Microarray data quantification and pre-processing was performed with the MAIA software and intensity values were log-transformed. Gene expression values were standardized across experiments with mean = 0 and standard deviation = 1. The SAM tool was applied to identify differentially expressed genes.
2011-01-29 | E-GEOD-26744 | biostudies-arrayexpress
Project description:Studies of miRNA profiling in early and late endothelial progenitor cells treated or not by cardioprotective nucleoside adenosine.
2011-03-15 | GSE27874 | GEO
Project description:Studies of miRNA profiling in early and late endothelial progenitor cells treated or not by cardioprotective nucleoside adenosine. Early outgrowth endothelial progenitor cells were obtained by adhesion of peripheral blood mononuclear cells of healthy volunteers. Late endothelial progenitor cells were obtained by purification of CD34+ peripheral blood cells and were cultured and amplified in endothelial-specific medium containing growth factors. Both cell types were treated by adenosine (10micromol/L) for 6 hours. Total RNA was extracted using mirVana Kit and quantified by Nanodrop. RNA was labeled and hybridized using Agilent miRNA Complete Labeling and Hyb Kit. 3 to 4 arrays per sample were hybridized and scanned with the Genepix 4000B Scanner (Molecular Devices). Six independent experiments were performed.
2011-03-15 | E-GEOD-27874 | biostudies-arrayexpress
Project description:Immunosuppression by adenosine is an important cancer immune checkpoint. Extracellular adenosine signals through specific receptors and can be transported across the cell membrane through nucleoside transporters. While adenosine receptors are well-known to regulate tumor immunity, the impact of adenosine transporters remains unexplored. In this study, we investigated the effect on tumor immunity of equilibrative nucleoside transporter-1 (ENT1), the major regulator of extracellular adenosine concentrations. Using selective inhibitors and gene targeting approaches, we demonstrated that blocking or deleting host ENT1 significantly enhanced CD8+ T cell-dependent anti-tumor responses. Tumors inoculated into ENT1-deficient mice showed increased infiltration of effector CD8+ T cells with an enhanced cytotoxic transcriptomic profile and significant upregulation of granzyme B, IFN-g, IL-2, TNF-a and CXCL10. ENT1-deficiency was further associated with decreased tumor-infiltrating T regulatory cells and CD206high macrophages, and suppressed CCL17 production. ENT1-deficiency notably potentiated the therapeutic activity of PD-1 blockade. T cells upregulated ENT1 upon activation, and blocking ENT1 enhanced their function when co-cultured with cognate antigen/HLA-matched melanoma cells. Mechanistically, ENT1-mediated adenosine uptake inhibited the activity of phosphoribosylpyrophosphate synthetase (PRPS) in activated T cells, thereby suppressing production of uridine 5′-monophosphate (UMP) and its derivatives required for DNA and RNA synthesis. In summary, our study identified ENT1-mediated adenosine uptake as an important and previously unappreciated mechanism of adenosine-mediated immunosuppression via pyrimidine starvation that can be targeted to enhance antitumor T cell responses.
2024-10-13 | GSE279144 | GEO
Project description:Epilepsy causes altered gene expression; transient adenosine treatment inhibits progression of epileptogenesis Hippocampus of epileptic rat is hypermethylated compared to naïve; adenosine treatment causes hypomethylation Metylation state in epileptic rats (9 weeks post kainic acid induced status epilepticus) was compared to naïve (untreated) rats and epileptic rats treated with adenosine for 5 days
2013-09-05 | E-GEOD-45932 | biostudies-arrayexpress
Project description:Epilepsy causes altered gene expression; transient adenosine treatment inhibits progression of epileptogenesis Hippocampus of epileptic rat is hypermethylated compared to naïve; adenosine treatment causes hypomethylation
2013-09-05 | GSE45932 | GEO
Project description:It is assumed that the anti-inflammatory nucleoside adenosine can shape immune responses by shifting the Treg/Th17 balance in favor of Tregs. This assumption is based on in vivo and vitro studies mostly performed in murine models and warrants confirmation in human models. In the study underlying these microarray data, we demonstrate that the pan-adenosine agonist 5'-N-ethylcarboxamidoadenosine (NECA) skews human CD3+ T cell responses towards non-inflammatory Th17 cells. We used microarrays to confirm transcriptome changes consistent with genetic signatures of non-pathogenic Th17 cells and to explore relevant metabolic pathways potentially contributing to this development.
2022-11-15 | GSE217911 | GEO
Project description:Colorectal cancer (CRC) is one of the common malignancies worldwide, accounting for a significant percentage of cancer mortality. Concurrent chemoradiation (CCRT) is now a standard treatment for unresectable malignancies of anorectum. To improve quality of life, CCRT is also commonly applied in treatment of lower rectal and anal canal cancer to preserve anal sphincter function. The most commonly used chemotherapeutic drugs combined with radiation as radiosensitizers is 5-fluorouracil (5-FU). Circulating endothelial progenitor cells (EPC), which contribute to the tumor vessel formation, reflect the response to chemotherapy both in animal model and clinical trial. Thus, circulating EPC can be used as a marker for optimizing and monitoring the anti-angiogenesis therapy including angiogenesis inhibitors and chemotherapy. Whether circulating EPC can be served as a marker of CCRT efficacy or not remains undetermined. Since CCRT is now a standard treatment of locally advanced and high-risk CRC, the development of a surrogate marker for monitoring CCRT response and optimize treatment intensity is very important.
In this grant we intent to monitor the levels of circulating EPC in locally advanced and high-risk CRC patients before, during and after CCRT. To further characterize the changes in function and biology of EPC caused by CCRT, a syngeneic animal model will be also used to evaluate the clonogenecity and specific gene expression of EPC in tumor-bearing mice receiving CCRT.
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Project description:HCT116 cells are treated by adenosine (4 mM) for 6 hours and then using total RNA for sequencing analysis to evaluate adenosine induced gene expression.
2023-11-29 | GSE216006 | GEO
Project description:The objective of this study was to reprogram peripheral blood-derived late-endothelial progenitor cells (EPCs) to a pluripotent state under feeder-free and defined culture conditions. Late-EPCs were retrovirally-transduced with OCT4, SOX2, KLF4, c-MYC, and iPSC colonies were derived in feeder-free and defined media conditions. EPC-iPSCs expressed pluripotent markers, were capable of differentiating to cells from all three germ-layers, and retained a normal karyotype. Transcriptome analyses demonstrated that EPC-iPSCs exhibit a global gene expression profile similar to human embryonic stem cells (hESCs). We have generated iPSCs from late-EPCs under feeder-free conditions. Thus, peripheral blood-derived late-outgrowth EPCs represent an alternative cell source for generating iPSCs. Six samples were analyzed. The gene expression profile of four iPS clones were compared to the H9 human embryonic stem cell line and the parent endothelial progenitor cell line.
2012-12-16 | E-GEOD-42947 | biostudies-arrayexpress