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Gene expression data from NECA (5/-N-ethylcarboxamidoadenosine) treated murine pituitary folliculostellate cells(TtT/GF)

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE15564 | GEO | 2009/04/08

SECONDARY ACCESSION(S): PRJNA115959

REPOSITORIES: GEO

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Gene expression data from NECA (5/-N-ethylcarboxamidoadenosine) treated murine pituitary folliculostellate cells(TtT/GF)

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

Gene expression profile in the heart of wild type and Adenosine Receptor A2a over expressing mice

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

Differential gene expression in activated microglia treated with adenosine A2A antagonists and A3 receptor agonists. A transcriptomics study.

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

Co-inhibition of CD73 and a2bar improves long-term cigarette smoke exposure impaired airway wound repair

Project description:Adenosine (ADO) involvement in lung injury depends on the activation of its receptors (A1, A2A, A2B, A3). The A2A receptor (A2AAR) and A2B receptor (A2BAR) are best described to have both tissue-protective and tissue-destructive processes. However, no approach has been effective in delineating the mechanism(s) involved with ADO shifting from its tissue-protective to tissue-destructive properties in chronic airway injury. Using cigarette smoke (CS) as our model of injury, we hypothesized that chronic CS exposure increases CD73-generated ADO which, activates low affinity A2BAR, subsequently impairing airway wound repair. To test this hypothesis, we chronically exposed human bronchial epithelial cell line, Nuli-1 cells, to 5% CS extract (CSE) for three years establishing a long-term CSE exposure model (LTC). We found significant morphological changes, decreased proliferation, and migration resulting in impaired airway wound closure in LTC. Further investigations showed that CSE exposure upregulates CD73 and A2BAR expression, increases ADO production, inhibits PKC alpha activity and phosphorylation of MEK, ERK, p90RSK and CREB. Moreover, when both or either of A2BAR and CD73 are knocked down in LTC, PKC alpha is activated and there is an increase in phosphorylation of MEK, ERK, p90RSK and CREB. Collectively, long-term CSE exposure upregulates CD73 expression and increases ADO production, which promotes A2BAR activation and subsequent diminution of PKC alpha activity and ERK signaling pathway, and inhibition of airway wound repair. Moreover, the data suggested that targeting both A2BAR and CD73 as potential therapeutic targets may be more efficacious in improving chronic CS impaired wound repair than either alone.

2020-10-08 | GSE111952 | GEO

IDO1 inhibition and subsequent metabolic adaptations constrains anti-tumor immune responses in the tumor microenvironment of patients with ovarian cancer

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

Effect of BAY60-6583 on gene expression of the SKOV-3 ovarian carcinoma cell line

Project description:The aim of this experiment is to analyze the regulation of gene expression by the A2B adenosine-receptor in ovarian carcinoma cells.

2021-10-28 | E-MTAB-11130 | biostudies-arrayexpress

Microarray analysis of a multiple myeloma cell line, MM1S, treated with adenosine A2A and Beta-2 Adrenergic Receptor agonists in combination with dexamethasone

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

Expression data from mouse bone marrow-derived macrophages (BMDMs)

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

Adenosine-treated endothelial progenitor cells

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

Parechovirus infection in human brain organoids: host innate inflammatory response and not neuro-infectivity correlates to neurologic disease

Project description:Picornaviruses are a leading cause of central nervous system (CNS) infections. While genotypes such as Parechovirus A3 (PeV-A3) and echovirus 11 (E11) can elicit severe neurological disease, the highly prevalent PeV-A1 is not associated with CNS disease. Here, we expand our current understanding of these differences in PeV-A CNS disease using human brain organoids and clinical isolates of PeV-A genotypes. Our data indicates that PeV-A1 and A3 specific differences in neurological disease are not due to infectivity of CNS cells as both viruses productively infect brain organoids with a similar cell tropism. Proteomic analysis showed that PeV-A infection significantly alters the host cell metabolism. The inflammatory response following PeV-A3 (and E11 infection) was significantly more potent than that upon PeV-A1 infection. Collectively, our findings align with clinical observations and suggest a role for inflammatory-mediated neurology, rather than viral replication, in PeV-A3 (and E11) infection.

2024-02-14 | PXD047238 | Pride

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