PMID: 17056121, 11111829 Under hypoxic conditions, the increased intracellular dephosphorylation of adenosine 5¡ì-triphosphate (ATP) to adenosine by the metabolic enzyme 5¡ì-nucleotidase is accompanied by a suppression of the activity of the salvage enzyme adenosine kinase, which prevents the rephosphorylation of adenosine.

PMID: 17056121, 10623851, 2581508, 11223861, 15019271 Adenosine accumulation is limited by its catabolism to inosine by adenosine deaminase. Inosine is finally degraded to the stable end product uric acid.

PMID: 17056121, 10623851, 2581508, 11223861, 15019271 Adenosine accumulation is limited by its catabolism to inosine by adenosine deaminase. Inosine is finally degraded to the stable end product uric acid.

PMID: 17056121 Lower concentrations of adenosine activate the high affinity A1, A2A, and A3 receptors, and high adenosine concentrations stimulate the low affinity A2B receptors.

PMID: 17056121 Lower concentrations of adenosine activate the high affinity A1, A2A, and A3 receptors, and high adenosine concentrations stimulate the low affinity A2B receptors.

PMID: 17056121 Lower concentrations of adenosine activate the high affinity A1, A2A, and A3 receptors, and high adenosine concentrations stimulate the low affinity A2B receptors.

PMID: 17056121 Lower concentrations of adenosine activate the high affinity A1, A2A, and A3 receptors, and high adenosine concentrations stimulate the low affinity A2B receptors.

PMID: 17056121, 956374 The first evidence supporting the concept that endogenous adenosine is capable of preventing human monocyte maturation was provided by demonstrating that adenosine deaminase activity is increased during early monocyte differentiation and that adenosine deaminase inhibition during this period delayed the maturation process. PMID: 17056121, 2159513 High concentrations of exogenous adenosine seem to prevent monocyte development into macrophages and arrest monocyte development at a stage with high accessory function, a phenotype that is similar to dendritic cells.

PMID: 17056121 The mechanism of action of adenosine involves induction, in a PKA-dependent manner, of the expression of p27kip-1, a cyclin-dependent kinase inhibitor that leads to growth arrest at the G1 phase of the cell cycle.

PMID: 17056121 The mechanism of action of adenosine involves induction, in a PKA-dependent manner, of the expression of p27kip-1, a cyclin-dependent kinase inhibitor that leads to growth arrest at the G1 phase of the cell cycle.

PMID: 17056121 The mechanism of action of adenosine involves induction, in a PKA-dependent manner, of the expression of p27kip-1, a cyclin-dependent kinase inhibitor that leads to growth arrest at the G1 phase of the cell cycle.

PMID: 17056121, 11111829 Under hypoxic conditions, the increased intracellular dephosphorylation of adenosine 5¡ì-triphosphate (ATP) to adenosine by the metabolic enzyme 5¡ì-nucleotidase is accompanied by a suppression of the activity of the salvage enzyme adenosine kinase, which prevents the rephosphorylation of adenosine.

PMID: 17056121, 15466916 When a small particle is coated (opsonized) with IgG, the Fc regions of the IgG antibody molecules bind to Fc receptors that are expressed on the macrophage plasma membrane and trigger a phagocytic response.

PMID: 17056121 In human monocytes, the non-selective adenosine receptor agonist 5¡ì-N-ethylcarboxamidoadenosine (NECA) but not 2-p-(2-carboxyethyl)phenethylamino-5¡ì-N-ethyl-carboxamidoadenosine (CGS 21680), a selective agonist of A2A receptors, down-regulated the proliferation of human peripheral blood mononuclear cells obtained from healthy subjects.

PMID: 17056121 In human monocytes, the non-selective adenosine receptor agonist 5¡ì-N-ethylcarboxamidoadenosine (NECA) but not 2-p-(2-carboxyethyl)phenethylamino-5¡ì-N-ethyl-carboxamidoadenosine (CGS 21680), a selective agonist of A2A receptors, down-regulated the proliferation of human peripheral blood mononuclear cells obtained from healthy subjects. PMID: 17056121, 10725262 On the other hand, the selective A1 receptor agonist N6-cyclopentyladenosine (CPA), but not other agonists, inhibited the proliferation of mononuclear cells in asthmatic patients.

PMID: 17056121, 10496321, 14977938 Two later studies, one using fMLP and the other LPS to stimulate oxidative burst, confirmed that the effect of adenosine could be attributed primarily to A3 receptor stimulation.

PMID: 17056121, 10496321, 14977938 Two later studies, one using fMLP and the other LPS to stimulate oxidative burst, confirmed that the effect of adenosine could be attributed primarily to A3 receptor stimulation.

PMID: 17056121, 8619882 Nitric oxide (NO) synthases (NOS) catalyze the oxidation of one of the guanidino nitrogens of l-arginine to the reactive nitrogen species NO. PMID: 17056121 Of the several NOS isoforms that can catalyze NO synthesis, iNOS is the primary one that is responsible for antimicrobial activity by producing high levels of NO. PMID: 17056121, 8906843 We demonstrated that both the selective A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) and A2A agonist CGS 21680 suppressed NO production by LPS-stimulated RAW264.7 macrophages, both with low efficacy.

PMID: 17056121, 1711326 Host expression of iNOS is first and foremost regulated at the transcriptional level and can be stimulated in response to microbial products or by cytokines such as IL-1, tumor necrosis factor-¦Á (TNF-¦Á) and interferon-¦Ã (IFN-¦Ã)

PMID: 17056121, 1711326 Host expression of iNOS is first and foremost regulated at the transcriptional level and can be stimulated in response to microbial products or by cytokines such as IL-1, tumor necrosis factor-¦Á (TNF-¦Á) and interferon-¦Ã (IFN-¦Ã)

PMID: 17056121, 1711326 Host expression of iNOS is first and foremost regulated at the transcriptional level and can be stimulated in response to microbial products or by cytokines such as IL-1, tumor necrosis factor-¦Á (TNF-¦Á) and interferon-¦Ã (IFN-¦Ã) PMID: 17056121, 10092821, 10510349 treatment of IFN-¦Ã-activated bone marrow macrophages with NECA decreased both iNOS induction and NO production in these cells.

PMID: 17056121, 11396612, 11396615 These processes lead to adenosine reaching high concentrations inside the cell and the release of adenosine into the extracellular space through nucleoside transporters.

PMID: 17056121, 8906843 We demonstrated that both the selective A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) and A2A agonist CGS 21680 suppressed NO production by LPS-stimulated RAW264.7 macrophages, both with low efficacy.

PMID: 17056121, 10092821, 10510349 treatment of IFN-¦Ã-activated bone marrow macrophages with NECA decreased both iNOS induction and NO production in these cells.

PMID: 17056121, 7945378 Stimulation of A2 receptors in U-937 human macrophages elicits VEGF mRNA accumulation. PMID: 17056121, 12057925 A2A receptor stimulation and LPS through TLR4 activation synergistically facilitated the production of VEGF.

PMID: 17056121, 7945378 Stimulation of A2 receptors in U-937 human macrophages elicits VEGF mRNA accumulation.

PMID: 17056121, 12057925 A2A receptor stimulation and LPS through TLR4 activation synergistically facilitated the production of VEGF.

PMID: 17056121, 12057925 A2A receptor stimulation and LPS through TLR4 activation synergistically facilitated the production of VEGF.

PMID: 17056121 Adenosine is a strong inhibitor of TNF-¦Á production by monocytes and macrophages. PMID: 17056121 IL-10 was also described as cytokine synthesis inhibitory factor, because IL-10 can inhibit the secretion of a variety of proinflammatory cytokines, including TNF-¦Á and IL-12

PMID: 17056121 Adenosine is a strong inhibitor of TNF-¦Á production by monocytes and macrophages. PMID: 17056121, 12875990 The inhibitory effect of adenosine on TNF-¦Á production by macrophages is not limited to TLR4-mediated (LPS) induction of this cytokine because adenosine down-regulates TNF-¦Á production when induced by agonists of TLR2, TLR3, TLR4, TLR7 and TLR9. PMID: 17056121 adenosine receptor agonists were shown to suppress TNF-¦Á production by LPS (TLR4 ligand)-challenged human monocytes with the following rank order of potency: NECA > R-PIA = CGS 21680 > 2-CADO (2-chloroadenosine) = CHA (N6-cyclohexyladenosine). PMID: 17056121, 11023991 In addition, CGS 21680 potently decreased TNF-¦Á production by A2A WT macrophages but it failed to influence TNF-¦Á release by KO cells.