Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA193678 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Adenosine binds to 4 G protein-coupled receptors located on the cardiomyocyte (A1-R, A2a-R, A2b-R and A3-R) and modulates cardiac function during both ischemia and load-induced stress. While the role of adenosine receptor-subtypes has been well defined in the setting of ischemia-reperfusion, far less is known regarding their roles in protecting the heart during other forms of cardiac stress. We characterized the gene expression profiles of heart from A2a-R over-expressing mice subjected to transverse aortic constriction to study the potential of A2a-R activation to protect from pressure-induced heart failure.
2015-03-22 | GSE45423 | GEO
Project description:Gene Expression Profile in thyroid of Transgenic Mice over-expressing the Adenosine Receptor 2a
| PRJNA87741 | ENA
Project description:To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a “danger” signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5’-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a “calm down” signal. If apoptotic cells produce “danger” or “anti-danger” signal(s), we rationalized that such signals would activate gene expression in macrophages. To investigate this possibility, we examined the effect of the culture supernatant from apoptotic cells on macrophage gene expression by using microarrays. For mouse BMDMs, bone marrow cells from female C57BL/6J mice at 8 weeks of age were cultured for more than 7 days with DMEM containing 10% FCS supplemented with mouse M-CSF. We used adherent cells as BMDMs in the study. W3 cells, mouse T cell line expressing Fas, were treated with human Fas ligand at 37°C for 30 min to induce apoptosis. The cells were then washed and re-suspended at a concentration of 1 × 107 cells/ml with RPMI containing 1% FCS, and further incubated for 60 min at 37°C. Following Fas ligand treatment, more than 90% of the W3 cells were Annexin V positive, and only small percentage were positive for both Annexin V and propidium iodide (PI). The culture supernatant was collected from apoptotic W3 cells. Next, BMDMs were incubated with medium (BMDMs-Medium) or apoptotic W3 cell supernatant (BMDMs-Apoptotic cell supernatant) for 1 h. Total RNA was extracted from the cells and hybridized on Affymetrix microarrays.
2014-06-24 | E-GEOD-50883 | biostudies-arrayexpress
Project description:We have used an agnostic approach to identify drug combinations by using combination high throughput screening (cHTS) technology and make the surprising discovery that adenosine A2A and beta-2 adrenergic receptor agonists are highly synergistic, selective and novel agents that enhance glucocorticoid activity in B-cell malignancies. We used the microarray study to understand the synergistic mechanism between dexamethasone and A2A receptor agonist or Beta-2 Adrenergic receptor agonist in a multiple myeloma cell line, MM1S. MM1S cells were treated with CGS-21680 or Salmeterol alone, or in combination with dexamethasone for six hours for RNA extraction and hybridization on Affymetrix microarrays.
2012-03-31 | E-GEOD-30644 | biostudies-arrayexpress
Project description:To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a “danger” signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5’-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a “calm down” signal. If apoptotic cells produce “danger” or “anti-danger” signal(s), we rationalized that such signals would activate gene expression in macrophages. To investigate this possibility, we examined the effect of the culture supernatant from apoptotic cells on macrophage gene expression by using microarrays.
2014-06-24 | GSE50883 | GEO
Project description:Microglial activation often accompanies the plastic changes occurring in the brain of patients with neurodegenerative diseases. A2A and A3 adenosine receptors have been proposed as therapeutic targets to combat neurodegeneration. RNAseq was performed using samples isolated from lipopolysaccharide/interferon-γ activated microglia treated with SCH 58261, a selective A2A receptor antagonist and 2-Cl-IB-MECA, a selective A3 receptor agonist.
2023-10-04 | GSE222696 | GEO
Project description:We have used an agnostic approach to identify drug combinations by using combination high throughput screening (cHTS) technology and make the surprising discovery that adenosine A2A and beta-2 adrenergic receptor agonists are highly synergistic, selective and novel agents that enhance glucocorticoid activity in B-cell malignancies. We used the microarray study to understand the synergistic mechanism between dexamethasone and A2A receptor agonist or Beta-2 Adrenergic receptor agonist in a multiple myeloma cell line, MM1S.
2012-04-01 | GSE30644 | GEO
Project description:Histone post-translational modifications (hPTMs) regulate gene expression via changes in chromatin accessibility and transcription factor recruitment. At a given locus, the coordinated enrichment of several distinct hPTMs regulate gene expression in response to external stimuli. However, neuronal hPTMs have been primarily characterized in bulk brain tissue and/or tissue pooled across subjects. This obscures both cell-type and individual variability, features essential to understand individual susceptibility to psychiatric disease. To address this limitation, we optimized a hybrid protocol, ICuRuS, to profile both activating and repressive hPTMs in a single neuronal subtype from a single mouse. We report here profiling of striatal medium spiny neuron (MSN) subtypes, genetically defined by expression of Adenosine 2a Receptor (A2a) or Dopamine Receptor D1 (D1), which differentially regulate reward processing and pathophysiology. Using ICuRuS, we defined genome-wide, A2a- or D1-specific combinatorial hPTM profiles, and discovered regulatory epigenomic features at genes implicated in neurobiological function and disease.
2022-11-17 | GSE193673 | GEO
Project description:To uncover underlying mechanisms associated with failure of indoleamine 2, 3-dioxygenase 1 (IDO1) blockade in clinical trials, we conducted a pilot, window-of-opportunity clinical study testing the immunological and metabolic effects of the IDO1 inhibitor, epacadostat, in seventeen patients with newly diagnosed advanced high grade serous ovarian cancer prior to their standard tumor debulking surgery. Comprehensive immunologic, transcriptomic, and metabolomic characterization of the tumor microenvironment using baseline and post-treatment tissue biopsies revealed efficient blockade of the kynurenine pathway of tryptophan degradation. This blockade was accompanied by a metabolic adaptation that shunted tryptophan catabolism towards the serotonin pathway and elevated nicotinamide adenine dinucleotide (NAD)+ biosynthetic pathways, which was detrimental for T cell proliferation and function. Treatment of mice bearing IDO1 over-expressing ovarian tumors with the NAMPT inhibitor, FK866, did not improve tumor control by epacadostat. Because NAD+ metabolites could be ligands for purinergic receptors, we investigated the impact of blocking purinergic receptors in the presence of NAD+. We demonstrated that A2a and A2b, or the combination of A2a and A2b purinergic receptor antagonists rescued NAD+-mediated suppression of T cell proliferation, and the combination of IDO inhibition and A2a/A2b receptor blockade improved survival in the IDO1 over-expressing ovarian tumor bearing hosts. These findings unravel previously unrecognized downstream adaptive metabolic consequences of IDO1 blockade that may undermine efforts to induce tumor-specific T cell responses.
2020-12-28 | GSE155164 | GEO
Project description:Folliculostellate cells constitute as much as 10% of the cells within the anterior pituitary gland; they however do not secrete any of the classical hormones but do express cytokines and growth factors. The endogenous nucleoside adenosine can be either pro- or anti-inflammatory depending on receptor expression and the activation of one or more receptors A1, A2a, A2b and A3. Adenosine stimulates the secretion of immune molecules from folliculostellate; these cells appear to mediate communication between the endocrine and immune systems. Replicate (x3) cultures of TtT/GF cells were treated with 10µM NECA (5/-N-ethylcarboxamidoadenosine) for 30 and 120 minutes. RNA was extracted, cRNA prepared and hybridized to murine MG_U74A v2 GeneChip (Affymetrix), changes in expression were compared with untreated controls.
2009-04-08 | E-GEOD-15564 | biostudies-arrayexpress