MiRNA profiling of Adenosine treated Endothelial Progenitor Cells (EPCs)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27874 | GEO | 2011/03/15
SECONDARY ACCESSION(S): PRJNA138007
REPOSITORIES: GEO
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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: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
2011-01-29 | GSE26744 | GEO
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:Endothelial progenitor cells (EPCs) are a group of cells which can differentiate to mature endothelial cells in a certain culture condition, and were first isolated from adult human peripheral blood by Asahara et al. in 1997. EPCs have a critical role in the restoration of injured vessel endothelium and the neovascularization in the area of ischemia injury. Recently, the role of androgens in the proliferation, differentiation and adhesion of EPCs is more and more focused. Dihydrotestosterone (DHT) is a kind of unmetabolizable androgen. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of regulated genes in DHT-treated EPCs.
2015-05-06 | GSE68541 | GEO
Project description:Endothelial progenitor cells (EPCs) are a group of cells which can differentiate to mature endothelial cells in a certain culture condition, and were first isolated from adult human peripheral blood by Asahara et al. in 1997. EPCs have a critical role in the restoration of injured vessel endothelium and the neovascularization in the area of ischemia injury. Recently, the role of androgens in the proliferation, differentiation and adhesion of EPCs is more and more focused. Dihydrotestosterone (DHT) is a kind of unmetabolizable androgen. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of regulated genes in DHT-treated EPCs. EPCs were isolated from mouse bone marrow. Male C57BL/6 mice (8 weeks age) mice were sacrificed by cervical dislocation. For microarray analysis, the cells were grown in culture medium supplemented with 10nmol/L DHT, which was changed on day 2. On day 7, cells was collected for RNA extraction and subsequent experiments.
2015-05-06 | E-GEOD-68541 | biostudies-arrayexpress
Project description:Evaluation of microRNA expression profile of microvesicles (MVs) derived from endothelial progenitor cells (EPCs) cultured in different oxygen concentrations (normoxic/hypoxic conditions)
2010-12-30 | E-MEXP-2956 | 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:BackgroundDue to their unique property to migrate to pathological lesions, stem cells are used as a delivery vehicle for therapeutic genes to tumors, especially for glioma. It is critically important to track the movement, localization, engraftment efficiency and functional capability or expression of transgenes of selected cell populations following transplantation. The purposes of this study were to investigate whether 1) intravenously administered, genetically transformed cord blood derived EPCs can carry human sodium iodide symporter (hNIS) to the sites of tumors in rat orthotopic model of human glioma and express transgene products, and 2) whether accumulation of these administered EPCs can be tracked by different in vivo imaging modalities.Methods and resultsCollected EPCs were cultured and transduced to carry hNIS. Cellular viability, differential capacity and Tc-99m uptake were determined. Five to ten million EPCs were intravenously administered and Tc-99-SPECT images were acquired on day 8, to determine the accumulation of EPCs and expression of transgenes (increase activity of Tc-99m) in the tumors. Immunohistochemistry was performed to determine endothelial cell markers and hNIS positive cells in the tumors. Transduced EPCs were also magnetically labeled and accumulation of cells was confirmed by MRI and histochemistry. SPECT analysis showed increased activity of Tc-99m in the tumors that received transduced EPCs, indicative of the expression of transgene (hNIS). Activity of Tc-99m in the tumors was also dependent on the number of administered transduced EPCs. MRI showed the accumulation of magnetically labeled EPCs. Immunohistochemical analysis showed iron and hNIS positive and, human CD31 and vWF positive cells in the tumors.ConclusionEPC was able to carry and express hNIS in glioma following IV administration. SPECT detected migration of EPCs and expression of the hNIS gene. EPCs can be used as gene carrier/delivery system for glioma therapy as well as imaging probes.
| S-EPMC3262815 | biostudies-literature
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:Bone marrow contains endothelial progenitor cells (EPCs) that, upon pro-angiogenic stimuli, migrate and differentiate into endothelial cells (ECs) and contribute to re-endothelialization and neo-vascularization. There are currently no reliable markers to characterize EPCs, leading to their inaccurate identification. In the past, we showed that, in a panel of tumors, some cells on the vessel wall co-expressed CD14 (monocytic marker) and CD31 (EC marker), indicating a putative differentiation route of monocytes into ECs. Herein, we disclosed monocytes as potential EPCs, using in vitro and in vivo models, and also addressed the cancer context. Monocytes acquired the capacity to express ECs markers and were able to be incorporated into blood vessels, contributing to cancer progression, by being incorporated in tumor neo-vasculature. Reactive oxygen species (ROS) push monocytes to EC differentiation, and this phenotype is reverted by cysteine (a scavenger and precursor of glutathione), which indicates that angiogenesis is controlled by the interplay between the oxidative stress and the scavenging capacity of the tumor microenvironment.
| S-EPMC7016533 | biostudies-literature