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Artículos de revistas sobre el tema "Adenosine A2B receptor"

Autor: Grafiati

Publicado: 10 de marzo de 2023

Última modificación: 31 de julio de 2025

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1

Wolska, Nina, and Marcin Rozalski. "Blood Platelet Adenosine Receptors as Potential Targets for Anti-Platelet Therapy." International Journal of Molecular Sciences 20, no. 21 (2019): 5475. http://dx.doi.org/10.3390/ijms20215475.

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Adenosine receptors are a subfamily of highly-conserved G-protein coupled receptors. They are found in the membranes of various human cells and play many physiological functions. Blood platelets express two (A2A and A2B) of the four known adenosine receptor subtypes (A1, A2A, A2B, and A3). Agonization of these receptors results in an enhanced intracellular cAMP and the inhibition of platelet activation and aggregation. Therefore, adenosine receptors A2A and A2B could be targets for anti-platelet therapy, especially under circumstances when classic therapy based on antagonizing the purinergic r

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2

Feng, Ming-Guo, and L. Gabriel Navar. "Afferent arteriolar vasodilator effect of adenosine predominantly involves adenosine A2B receptor activation." American Journal of Physiology-Renal Physiology 299, no. 2 (2010): F310—F315. http://dx.doi.org/10.1152/ajprenal.00149.2010.

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Adenosine is an important paracrine agent regulating renal vascular tone via adenosine A1 and A2 receptors. While A2B receptor message and protein have been localized to preglomerular vessels, functional evidence on the role of A2B receptors in mediating the vasodilator action of adenosine on afferent arterioles is not available. The present study determined the role of A2B receptors in mediating the afferent arteriolar dilation and compared the effects of A2B and A2A receptor blockade on afferent arterioles. We used the rat in vitro blood-perfused juxtamedullary nephron technique combined wit

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3

Gebremedhin, Debebe, Brian Weinberger, David Lourim, and David R. Harder. "Adenosine Can Mediate its Actions through Generation of Reactive Oxygen Species." Journal of Cerebral Blood Flow & Metabolism 30, no. 10 (2010): 1777–90. http://dx.doi.org/10.1038/jcbfm.2010.70.

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Adenosine is an important cerebral vasodilator, but mediating mechanisms are not understood. We investigated the expression of adenosine receptor subtypes in isolated cerebral arterial muscle cells (CAMCs), and their role in adenosine-induced superoxide (O2−) generation and reduction in cerebral arterial tone. Reverse transcriptase-PCR, western blotting, and immunofluorescence studies have shown that CAMCs express transcript and protein for A1, A2A, A2B, and A3 adenosine receptors. Stimulation of CAMCs with adenosine or the A2A agonist CGS-21680 increased the generation of O2− that was attenua

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4

Zaynagetdinov, Rinat, Kai Schiemann, Kalyan Nallaparaju, et al. "Abstract 3499: M1069 as dual A2A/A2B adenosine receptor antagonist counteracts immune-suppressive mechanisms of adenosine and reduces tumor growth in vivo." Cancer Research 82, no. 12_Supplement (2022): 3499. http://dx.doi.org/10.1158/1538-7445.am2022-3499.

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Abstract Under physiological conditions, the extracellular concentrations of adenosine are low, however, levels dramatically increase under metabolically stressful conditions, including inflammation and cancer. The regulatory functions of adenosine are mediated through four members of the adenosine receptor family: A1, A2A, A2B, and A3. While A2A was considered the major contributor to adenosine-mediated suppression of T cell, natural killer cell, and myeloid cell functions, A2B has also recently emerged as a potential modulator of these processes. Both A2A and A2B signal through the same Gs-m

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5

Xaus, Jordi, Maribel Mirabet, Jorge Lloberas та ін. "IFN-γ Up-Regulates the A2B Adenosine Receptor Expression in Macrophages: A Mechanism of Macrophage Deactivation". Journal of Immunology 162, № 6 (1999): 3607–14. http://dx.doi.org/10.4049/jimmunol.162.6.3607.

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Abstract Adenosine is a potent endogenous anti-inflammatory agent released by cells in metabolically unfavorable conditions, such as hypoxia or ischemia. Adenosine modulates different functional activities in macrophages. Some of these activities are believed to be induced through the uptake of adenosine into the macrophages, while others are due to the interaction with specific cell surface receptors. In murine bone marrow-derived macrophages, the use of different radioligands for adenosine receptors suggests the presence of A2B and A3 adenosine receptor subtypes. The presence of A2B receptor

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6

Shi, Yanrong, Xiaoguang Liu, Debebe Gebremedhin, John R. Falck, David R. Harder, and Raymond C. Koehler. "Interaction of Mechanisms Involving Epoxyeicosatrienoic Acids, Adenosine Receptors, and Metabotropic Glutamate Receptors in Neurovascular Coupling in Rat Whisker Barrel Cortex." Journal of Cerebral Blood Flow & Metabolism 28, no. 1 (2007): 111–25. http://dx.doi.org/10.1038/sj.jcbfm.9600511.

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Adenosine, astrocyte metabotropic glutamate receptors (mGluRs), and epoxyeicosatrienoic acids (EETs) have been implicated in neurovascular coupling. Although A2A and A2B receptors mediate cerebral vasodilation to adenosine, the role of each receptor in the cerebral blood flow (CBF) response to neural activation remains to be fully elucidated. In addition, adenosine can amplify astrocyte calcium, which may increase arachidonic acid metabolites such as EETs. The interaction of these pathways was investigated by determining if combined treatment with antagonists exerted an additive inhibitory eff

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7

Marquardt, D. L., L. L. Walker, and S. Heinemann. "Cloning of two adenosine receptor subtypes from mouse bone marrow-derived mast cells." Journal of Immunology 152, no. 9 (1994): 4508–15. http://dx.doi.org/10.4049/jimmunol.152.9.4508.

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Abstract Adenosine potentiates the stimulated release of mast cell mediators. Pharmacologic studies suggest the presence of two adenosine receptors, one positively coupled to adenylate cyclase and the other coupled to phospholipase C activation. To identify mast cell adenosine receptor subtypes, cDNAs for the A1 and A2a adenosine receptors were obtained by screening a mouse brain cDNA library with the use of PCR-derived probes. Mouse bone marrow-derived mast cell cDNA libraries were constructed and screened with the use of A1 and A2a cDNA probes, which revealed the presence of A2a, but not A1,

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8

Dubey, Raghvendra K., Delbert G. Gillespie, and Edwin K. Jackson. "A2B Adenosine Receptors Mediate the Anti-Mitogenic Effects of Adenosine in Cardiac Fibroblasts." Hypertension 36, suppl_1 (2000): 708. http://dx.doi.org/10.1161/hyp.36.suppl_1.708-b.

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P85 Adenosine inhibits growth of CFs; however, the adenosine receptor subtype that mediates this anti-mitogenic effect remains undefined. Using specific ADE receptor antagonists and agonists and antisense oligonucleotides (OLIGO) against A2B receptors, we investigated the role of A2B receptors in inhibiting cardiac fibroblast growth. PDGF (25ng/ml)-induced DNA synthesis, cell number and collagen synthesis in CFs were inhibited by A2 (chloroadenosine [Cl-Ad]and MECA), but not by A1 (CPA), A2a ( CGS21680 ) or A3 (AB-MECA),receptor agonists.The inhibitory effects of 1μM MECA and Cl-Ad were revers

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9

Zhan, Enbo, Victoria J. McIntosh, and Robert D. Lasley. "Adenosine A2A and A2B receptors are both required for adenosine A1 receptor-mediated cardioprotection." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (2011): H1183—H1189. http://dx.doi.org/10.1152/ajpheart.00264.2011.

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All four adenosine receptor subtypes have been shown to play a role in cardioprotection, and there is evidence that all four subtypes may be expressed in cardiomyocytes. There is also increasing evidence that optimal adenosine cardioprotection requires the activation of more than one receptor subtype. The purpose of this study was to determine whether adenosine A2A and/or A2B receptors modulate adenosine A1 receptor-mediated cardioprotection. Isolated perfused hearts of wild-type (WT), A2A knockout (KO), and A2BKO mice, perfused at constant pressure and constant heart rate, underwent 30 min of

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10

Lu, Qing, Elizabeth O. Harrington, Julie Newton, et al. "Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancement." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 6 (2010): L755—L767. http://dx.doi.org/10.1152/ajplung.00330.2009.

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We have previously demonstrated that adenosine plus homocysteine enhanced endothelial basal barrier function and protected against agonist-induced barrier dysfunction in vitro through attenuation of RhoA activation by inhibition of isoprenylcysteine-O-carboxyl methyltransferase. In the current study, we tested the effect of elevated adenosine on pulmonary endothelial barrier function in vitro and in vivo. We noted that adenosine alone dose dependently enhanced endothelial barrier function. While adenosine receptor A1 or A3 antagonists were ineffective, an adenosine transporter inhibitor, NBTI,

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11

Kreisberg, M. S., E. P. Silldorff, and T. L. Pallone. "Localization of adenosine-receptor subtype mRNA in rat outer medullary descending vasa recta by RT-PCR." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (1997): H1231—H1238. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1231.

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Adenosine has a multitude of functions in the kidney, including vasoregulation of the renal vasculature. The actions of adenosine are mediated by its binding to specific receptors. Four adenosine-receptor subtypes have been cloned and sequenced, the A1, A2a, A2b, and the A3. In this study, the expression of individual adenosine-receptor subtype RNAs in outer medullary descending vasa recta (OMDVR) was investigated. Total RNA isolated from the outer medulla and microdissected, permeabilized OMDVR were subjected to reverse transcription-polymerase chain reaction (RT-PCR) with primers specific fo

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12

Cekic, Caglar, and Joel Linden. "Adenosine A2B receptor signaling in antigen presenting cells suppress anti-tumor adaptive immune responses (127.10)." Journal of Immunology 188, no. 1_Supplement (2012): 127.10. http://dx.doi.org/10.4049/jimmunol.188.supp.127.10.

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Abstract Adenosine is generated in response to cellular stress such as hypoxia and inflammation and acts as a “metabokine” to modulate immune responses and prevent tissue damage. The accumulation of high levels of adenosine in tumors activates adenosine A2A and A2B receptors on immune cells to attenuate tumor rejection. Previously, we have shown that A2BR blockade inhibits growth of syngeneic tumors by enhancing innate and adaptive immune responses. However, the cellular targets that mediate inhibition of tumor growth after A2B receptor blockade are unknown. In this study, we tested the activi

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13

Borgland, Stephanie L., Maria Castañón, Walter Spevak, and Fiona E. Parkinson. "Effects of propentofylline on adenosine receptor activity in Chinese hamster ovary cell lines transfected with human A1, A2A, or A2B receptors and a luciferase reporter gene." Canadian Journal of Physiology and Pharmacology 76, no. 12 (1998): 1132–38. http://dx.doi.org/10.1139/y98-143.

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Propentofylline is neuroprotective in vivo, but its mechanism of action is not completely understood. Previously, propentofylline was shown to block adenosine transport processes, to inhibit three adenosine receptor subtypes, and to inhibit cAMP phosphodiesterase. We tested the effect of propentofylline on adenosine receptor function in Chinese hamster ovary (CHO) cells transfected with human adenosine A1, A2A, or A2B receptors and a luciferase reporter gene under control of a promoter sequence containing several copies of the cAMP response element. We investigated the concentration-dependent

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14

Xiang, Hong-Jun, Fu-Lu Chai, De-Sheng Wang, and Ke-Feng Dou. "Downregulation of the Adenosine A2b Receptor by RNA Interference Inhibits Hepatocellular Carcinoma Cell Growth." ISRN Oncology 2011 (April 28, 2011): 1–7. http://dx.doi.org/10.5402/2011/875684.

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To investigate the biological effect of adenosine A2b receptor (A2bR) on the human hepatocellular carcinoma cell line HepG2, three A2bR siRNA constructs were transiently transfected into HepG2 cells. The results showed that A2bR siRNA reduced the levels of A2bR mRNA and protein. In order to further detect the function of A2bR, we established a stable hepatocellular carcinoma cell line (HepG2) expressing siRNA targeting the adenosine A2b receptor. Targeted RNAi significantly inhibited tumor cell growth in vitro, and flow cytometry (FCM) showed that significantly more cells expressing A2bR siRNA

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15

Olanrewaju, Hammed A., W. Qin, I. Feoktistov, Jean-Luc Scemama, and S. Jamal Mustafa. "Adenosine A2A and A2B receptors in cultured human and porcine coronary artery endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 2 (2000): H650—H656. http://dx.doi.org/10.1152/ajpheart.2000.279.2.h650.

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We investigated the role of the cAMP link to the signal transduction mechanism coupled with adenosine A2A and A2Breceptors in cultured human coronary artery endothelial cells (HCAEC) and porcine coronary artery endothelial cells (PCAEC). 2-[4-[2-{2-[(4-aminophenyl)methylcarbonylamino]ethylaminocarbonyl}ethyl]phenyl]ethylamino-5′- ethylcarboxamidoadenosine (125I-PAPA-APEC) (PAPA-APEC) was used to demonstrate the specific binding in PCAEC membranes. The specific binding was saturable and reversible with a maximal number of binding sites (Bmax) of 240 fmol/mg protein, and scatchard analysis revea

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Darlington, Daniel N., Xiaowu Wu, Kevin L. Chang, James Bynum, and Andrew P. Cap. "Regulation of Platelet Function By Adenosine Receptors." Blood 134, Supplement_1 (2019): 2348. http://dx.doi.org/10.1182/blood-2019-131129.

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Introduction: We have recently shown that severe trauma and hemorrhage lead to inhibition of platelet aggregation and an elevation in cyclic adenosine monophosphate (cAMP). Adenosine is one of the few humoral agents known to stimulate cAMP in platelets. Because adenosine is released from damaged tissue, it may contribute to the platelet dysfunction seen after severe trauma. Platelets have four adenosine receptors (A1, A2a, A2b and A3). These receptors are G-Protein Coupled Receptors and have been proposed to stimulate adenylyl cyclase and increase intracellular cAMP. Although studies have show

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Csoka, Balazs, Balazs Koscso, Gabor Toro, et al. "A2B adenosine receptors inhibit obesity-induced adipose tissue inflammation (P3109)." Journal of Immunology 190, no. 1_Supplement (2013): 43.16. http://dx.doi.org/10.4049/jimmunol.190.supp.43.16.

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Abstract Obesity promotes adipose tissue inflammation, which in turn causes insulin resistance in target organs by dysregulation of adipokine release and by increased classical and decreased alternative macrophage activation. Because A2B adenosine receptors are important regulators of macrophage activation, we examined the role of A2B adenosine receptors in diet-induced inflammation and insulin resistance. A2B receptor deletion impaired glucose metabolism in mice fed chow but not high fat diet. This impaired glucose homeostasis in A2B receptor deficient mice was paralleled by increased classic

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18

Cekic, Caglar, Ali Can Savas, Merve Kayhan, Altay Koyas, and Imran Akdemir. "Targeting adenosine A2A receptors to improve vaccine efficacy." Journal of Immunology 198, no. 1_Supplement (2017): 79.22. http://dx.doi.org/10.4049/jimmunol.198.supp.79.22.

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Abstract Activation of immune cells is associated with increased expression of adenosine receptors. Extracellular adenosine is present in primary and secondary lymphoid organs and limit the amplitude of immune responses suggesting that antagonists for adenosine receptors can be targeted to improve the efficacy of vaccines. Here we showed that vaccine adjuvant Monophosphoryl Lipid A (MPLA) strongly increased adenosine A2A and adenosine A2B receptor expression in primary macrophages and dendritic cells. Adenosine A2A but not adenosine A2B receptor blockade significantly increased both numbers an

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Allen-Gipson, Diane S., Michael R. Blackburn, Daniel J. Schneider, et al. "Adenosine activation of A2B receptor(s) is essential for stimulated epithelial ciliary motility and clearance." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 2 (2011): L171—L180. http://dx.doi.org/10.1152/ajplung.00203.2010.

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Mucociliary clearance, vital to lung clearance, is dependent on cilia beat frequency (CBF), coordination of cilia, and the maintenance of periciliary fluid. Adenosine, the metabolic breakdown product of ATP, is an important modulator of ciliary motility. However, the contributions of specific adenosine receptors to key airway ciliary motility processes are unclear. We hypothesized that adenosine modulates ciliary motility via activation of its cell surface receptors (A1, A2A, A2B, or A3). To test this hypothesis, mouse tracheal rings (MTRs) excised from wild-type and adenosine receptor knockou

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Teng, Bunyan, Daniel N. Darlington, and Andrew P. Cap. "Adenosine Receptor Identification for Controlling Platelet Aggregation." Blood 132, Supplement 1 (2018): 3733. http://dx.doi.org/10.1182/blood-2018-99-116213.

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Abstract Introduction: Adenosine, an autacoid and metabolite of ATP, has been known to have anti-platelet properties. Of the 4 adenosine receptors, both A2A and/or A2B have been implicated in adenosine-mediated anti-platelet properties, while the roles of A1 and A3 have not been clearly defined in humans. In addition, previous studies show that A2A/A2B on platelets are G-Protein Coupled Receptors and are coupled to a stimulatory G-protein that activate adenylyl cyclase and subsequently increase intracellular cAMP. An elevation of cAMP in platelets inhibits aggregation. In this study, we set ou

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Ruiz-García, Almudena, Eva Monsalve, Laura Novellasdemunt, et al. "Cooperation of Adenosine with Macrophage Toll-4 Receptor Agonists Leads to Increased Glycolytic Flux through the Enhanced Expression of PFKFB3 Gene." Journal of Biological Chemistry 286, no. 22 (2011): 19247–58. http://dx.doi.org/10.1074/jbc.m110.190298.

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Macrophages activated through Toll receptor triggering increase the expression of the A2A and A2B adenosine receptors. In this study, we show that adenosine receptor activation enhances LPS-induced pfkfb3 expression, resulting in an increase of the key glycolytic allosteric regulator fructose 2,6-bisphosphate and the glycolytic flux. Using shRNA and differential expression of A2A and A2B receptors, we demonstrate that the A2A receptor mediates, in part, the induction of pfkfb3 by LPS, whereas the A2B receptor, with lower adenosine affinity, cooperates when high adenosine levels are present. pf

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Han, Sandong, Nam Hee Kim, Hongmei He, and Zhi Liang Chu. "Abstract LB166: Discovery of CT3021, a novel potent adenosine A2a/A2b/A1 receptor triple antagonist." Cancer Research 84, no. 7_Supplement (2024): LB166. http://dx.doi.org/10.1158/1538-7445.am2024-lb166.

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Abstract In a CD73-positive tumor microenvironment (TME), ATP released from apoptotic tumor cells converts to adenosine, generating an adenosine-rich immunosuppressive environment. Adenosine activates G-protein coupled receptors expressed on immune cells to achieve immune suppression, with a mechanism of action involving 1) dampening antitumor effector cells (T eff and NK cells) via adenosine engagement on A2a receptor, (2) reducing dendritic cell antigen presentation and promoting MDSC differentiation by activating A2b and A2a receptors, and (3) inducing chemotactic migration of immature plas

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Mirabet, M., C. Herrera, O. J. Cordero, J. Mallol, C. Lluis, and R. Franco. "Expression of A2B adenosine receptors in human lymphocytes: their role in T cell activation." Journal of Cell Science 112, no. 4 (1999): 491–502. http://dx.doi.org/10.1242/jcs.112.4.491.

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Extracellular adenosine has a key role in the development and function of the cells of the immune system. Many of the adenosine actions seem to be mediated by specific surface receptors positively coupled to adenylate cyclase: A2A and A2B. Despite the fact that A2A receptors (A2ARs) can be easily studied due to the availability of the specific agonist CGS21680, a pharmacological and physiological characterization of adenosine A2B receptors (A2BRs) in lymphocytes has not been possible due to the lack of suitable reagents. Here we report the generation and characterization of a polyclonal antipe

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Fan, Ming, Weixi Qin, and S. Jamal Mustafa. "Characterization of adenosine receptor(s) involved in adenosine-induced bronchoconstriction in an allergic mouse model." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 6 (2003): L1012—L1019. http://dx.doi.org/10.1152/ajplung.00353.2002.

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We recently reported that adenosine caused bronchoconstriction and enhanced airway inflammation in an allergic mouse model. In this study, we further report the characterization of the subtype of adenosine receptor(s) involved in bronchoconstriction. 5′-( N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist, elicited bronchoconstriction in a dose-dependent manner. Little effects of N 6-cyclopentyladenosine (A1-selective agonist) and 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamidoadenosine (A2A-selective agonist) compared with NECA were observed in this model. 2-Chlo

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Areias, Filipe, Carla Correia, Ashly Rocha, et al. "2-Aryladenine Derivatives as a Potent Scaffold for Adenosine Receptor Antagonists: The 6-Morpholino Derivatives." Molecules 29, no. 11 (2024): 2543. http://dx.doi.org/10.3390/molecules29112543.

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A set of 2-aryl-9-H or methyl-6-morpholinopurine derivatives were synthesized and assayed through radioligand binding tests at human A1, A2A, A2B, and A3 adenosine receptor subtypes. Eleven purines showed potent antagonism at A1, A3, dual A1/A2A, A1/A2B, or A1/A3 adenosine receptors. Additionally, three compounds showed high affinity without selectivity for any specific adenosine receptor. The structure-activity relationships were made for this group of new compounds. The 9-methylpurine derivatives were generally less potent but more selective, and the 9H-purine derivatives were more potent bu

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Chen, Yinghong, Sara Epperson, Lala Makhsudova, et al. "Functional effects of enhancing or silencing adenosine A2b receptors in cardiac fibroblasts." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 6 (2004): H2478—H2486. http://dx.doi.org/10.1152/ajpheart.00217.2004.

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Cardiac fibroblasts (CF) express adenosine (ADO) receptors, and pharmacological evidence suggests the possible involvement of the A2 (A2a and A2b) receptor (A2aR and A2bR) subtypes in inhibiting cell functions involved in fibrosis. The main objective of this study was to define the contributions of A2a and/or A2b receptors in modulating ADO-induced decreases in CF functions. For this purpose, CF were either treated pharmacologically or had the A2aR or A2bR levels modified through the use of recombinant adenovirus or siRNA. The assessment of mRNA expression in adult rat CF yielded evidence for

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Ngai, Al C., Ellicia F. Coyne, Joseph R. Meno, G. Alexander West, and H. Richard Winn. "Receptor subtypes mediating adenosine-induced dilation of cerebral arterioles." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (2001): H2329—H2335. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2329.

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The purpose of this study was to investigate the receptor subtypes that mediate the dilation of rat intracerebral arterioles elicited by adenosine. Penetrating arterioles were isolated from the rat brain, cannulated with the use of a micropipette system, and luminally pressurized to 60 mmHg. Both adenosine and the A2A receptor-selective agonist CGS-21680 induced dose-dependent vasodilation (−logEC50: 6.5 ± 0.2 and 8.6 ± 0.3, respectively). However, adenosine, which is capable of activating both A2A and A2B receptors, caused a greater maximal dilation than CGS-21680. The A2Areceptor-selective a

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Hassanian, Seyed Mahdi, and Alireza R. Rezaie. "Adenosine Inhibits Pro-Inflammatory Thrombin Signaling In Endothelial Cells." Blood 122, no. 21 (2013): 1064. http://dx.doi.org/10.1182/blood.v122.21.1064.1064.

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Abstract Adenosine is an important regulatory metabolite which attenuates inflammation when it binds and activates the adenosine A2A receptor subtype on immune cells. However, the effect of adenosine on inflammatory responses in endothelial cells is mostly unknown. Thrombin as a known pro-inflammatory protease is involved in a variety of pathophysiological processes associated with inflammation in stimulated endothelial cells. The present study investigated the effect of adenosine on thrombin-mediated modulation of pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs).

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Garcia-Garcia, Lucia, Laia Olle, Margarita Martin, Jordi Roca-Ferrer, and Rosa Muñoz-Cano. "Adenosine Signaling in Mast Cells and Allergic Diseases." International Journal of Molecular Sciences 22, no. 10 (2021): 5203. http://dx.doi.org/10.3390/ijms22105203.

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Adenosine is a nucleoside involved in the pathogenesis of allergic diseases. Its effects are mediated through its binding to G protein-coupled receptors: A1, A2a, A2b and A3. The receptors differ in the type of G protein they recruit, in the effect on adenylyl cyclase (AC) activity and the downstream signaling pathway triggered. Adenosine can produce both an enhancement and an inhibition of mast cell degranulation, indicating that adenosine effects on these receptors is controversial and remains to be clarified. Depending on the study model, A1, A2b, and A3 receptors have shown anti- or pro-in

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Franco, Rafael, Rafael Rivas-Santisteban, Gemma Navarro, and Irene Reyes-Resina. "Adenosine Receptor Antagonists to Combat Cancer and to Boost Anti-Cancer Chemotherapy and Immunotherapy." Cells 10, no. 11 (2021): 2831. http://dx.doi.org/10.3390/cells10112831.

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Extracellular adenosine accumulates in the environment of numerous tumors. For years, this fact has fueled preclinical research to determine whether adenosine receptors (ARs) could be the target to fight cancer. The four ARs discovered so far, A1, A2A, A2B and A3, belong to the class A family of G protein-coupled receptors (GPCRs) and all four have been involved in one way or another in regulating tumor progression. Prompted by the successful anti-cancer immunotherapy, the focus was placed on the ARs more involved in regulation of immune cell differentiation and activation and that are able to

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Arin, Rosa María, Ana Isabel Vallejo, Yuri Rueda, Olatz Fresnedo, and Begoña Ochoa. "Stimulation of gastric acid secretion by rabbit parietal cell A2B adenosine receptor activation." American Journal of Physiology-Cell Physiology 309, no. 12 (2015): C823—C834. http://dx.doi.org/10.1152/ajpcell.00224.2015.

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Adenosine modulates different functional activities in many cells of the gastrointestinal tract; some of them are believed to be mediated by interaction with its four G protein-coupled receptors. The renewed interest in the adenosine A2B receptor (A2BR) subtype can be traced by studies in which the introduction of new genetic and chemical tools has widened the pharmacological and structural knowledge of this receptor as well as its potential therapeutic use in cancer and inflammation- or hypoxia-related pathologies. In the acid-secreting parietal cells of the gastric mucosa, the use of various

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Cekic, Caglar, Duygu Sag, and Joel Linden. "Aminophylline inhibits breast and bladder tumor growth in mice due to CXCR3-dependent adenosine A2B receptor blockade (165.32)." Journal of Immunology 186, no. 1_Supplement (2011): 165.32. http://dx.doi.org/10.4049/jimmunol.186.supp.165.32.

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Abstract The activation of adenosine A2A or A2B receptors on immune cells inhibits their ability to suppress tumor growth. In this study, we evaluated the anti-tumor effects of aminophyllilne (AMO) a nonselective antagonist of A2A and A2B receptors that is used clinically to treat asthma. Intra-tumor injection of AMO inhibited the growth of syngeneic MB49 bladder cells subcutaneously injected into C57BL/6 mice and the growth and lung metastasis of luminescent syngeneic 4T1 breast tumor cells inoculated into the mammary fat pats of Balb/c mice. Although AMO inhibited the growth of MB49 in A2AR-

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Sharif, Ehesan U., Dillon H. Miles, Brandon R. Rosen, et al. "Abstract PR001: Discovery of Etrumadenant, a first-in-class dual A2a and A2b adenosine receptor antagonist for cancer immunotherapy." Molecular Cancer Therapeutics 23, no. 12_Supplement (2024): PR001. https://doi.org/10.1158/1538-8514.cancerchem24-pr001.

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Abstract High levels of adenosine are generated in the tumor microenvironment (TME) by sequential hydrolysis of extracellular ATP by the ecto-nucleotidases CD39 (ATP→AMP) and CD73 (AMP→adenosine). Adenosine activates A2a and A2b adenosine receptors on immune cells, resulting in immunosuppression. Since A2aR is expressed by a variety of lymphocytes, the suppressive effects of adenosine on this cell type can be potentially reversed by blocking the A2aR. In contrast, myeloid cells that have comparable expression of A2aR and A2bR require dual A2a/bR blockade for full reversal of the immunosuppress

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Kotańska, Magdalena, Anna Dziubina, Małgorzata Szafarz, et al. "Preliminary Evidence of the Potent and Selective Adenosine A2B Receptor Antagonist PSB-603 in Reducing Obesity and Some of Its Associated Metabolic Disorders in Mice." International Journal of Molecular Sciences 23, no. 21 (2022): 13439. http://dx.doi.org/10.3390/ijms232113439.

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The adenosine A2A and A2B receptors are promising therapeutic targets in the treatment of obesity and diabetes since the agonists and antagonists of these receptors have the potential to positively affect metabolic disorders. The present study investigated the link between body weight reduction, glucose homeostasis, and anti-inflammatory activity induced by a highly potent and specific adenosine A2B receptor antagonist, compound PSB-603. Mice were fed a high-fat diet for 14 weeks, and after 12 weeks, they were treated for 14 days intraperitoneally with the test compound. The A1/A2A/A2B recepto

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DeMong, Duane E., Sheila Ranganath, Jared Cumming, et al. "Abstract IA013: Discovery of the dual A2A/A2B receptor antagonist MK-1088 for the treatment of solid tumors." Molecular Cancer Therapeutics 23, no. 12_Supplement (2024): IA013. https://doi.org/10.1158/1538-8514.cancerchem24-ia013.

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Abstract In the tumor microenvironment (TME), adenosine levels have been shown to be elevated relative to normal tissues. This increase in adenosine levels renders an immunosuppressive effect via direct effects on T cells via agonism of the A2A receptor and indirect effects via agonism of both A2A and A2B receptors on myeloid cells. With these observations as a backdrop, we sought to develop a dual A2A/A2B receptor antagonist with properties that would enable maintenance of high levels of target engagement of the A2A and A2B receptors even at trough concentration. Drawing on our organization’s

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Rees, D. A., M. D. Lewis, B. M. Lewis, P. J. Smith, M. F. Scanlon, and J. Ham. "Adenosine-Regulated Cell Proliferation in Pituitary Folliculostellate and Endocrine Cells: Differential Roles for the A1 and A2B Adenosine Receptors." Endocrinology 143, no. 6 (2002): 2427–36. http://dx.doi.org/10.1210/endo.143.6.8837.

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Abstract A1 and A2 adenosine receptors have been identified in the pituitary gland, but the cell type(s) on which they are located and their effects on pituitary cell growth are not known. Therefore, we analyzed the expression of A1 and A2 receptors in primary rat anterior pituitary cells, two pituitary folliculostellate (TtT/GF and Tpit/F1) and two pituitary endocrine (GH3 and AtT20) cell lines, and compared their effects on cell proliferation. In anterior pituitary and folliculostellate cells, adenosine and adenosine receptor agonists (5′-N-ethylcarboxamidoadenosine, a universal agonist, and

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Remley, Victoria A., Joel Linden, Todd W. Bauer, and Julien Dimastromatteo. "Unlocking antitumor immunity with adenosine receptor blockers." Cancer Drug Resistance 6, no. 4 (2023): 748–67. http://dx.doi.org/10.20517/cdr.2023.63.

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Tumors survive by creating a tumor microenvironment (TME) that suppresses antitumor immunity. The TME suppresses the immune system by limiting antigen presentation, inhibiting lymphocyte and natural killer (NK) cell activation, and facilitating T cell exhaustion. Checkpoint inhibitors like anti-PD-1 and anti-CTLA are immunostimulatory antibodies, and their blockade extends the survival of some but not all cancer patients. Extracellular adenosine triphosphate (ATP) is abundant in inflamed tumors, and its metabolite, adenosine (ADO), is a driver of immunosuppression mediated by adenosine A2A rec

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Koscso, Balazs, Zsolt Selmeczy, Leonora Himer, Balazs Csoka, and Gyorgy Hasko. "Adenosine receptor activation augments IL-10 production by murine microglial cells (116.31)." Journal of Immunology 186, no. 1_Supplement (2011): 116.31. http://dx.doi.org/10.4049/jimmunol.186.supp.116.31.

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Abstract Microglia, the intrinsic macrophages of the central nervous system produce the anti-inflammatory cytokine IL-10 following activation with the bacterial cell wall product peptidoglycan (PGN), which is recognized by Toll-like receptor 2 (TLR2). Adenosine is an endogenous purine nucleoside that binds to specific G protein-coupled receptors (A1, A2A, A2B, and A3), and is a well known modulator of the immune system. In this study we investigated the effect of adenosine on IL-10 production by microglia. Cells were treated with adenosine, or selective adenosine receptor agonists and antagoni

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Baraldi, P. G., B. Cacciar, G. Spalluto, et al. "Current Developments of A2a Adenosine Receptor Antagonists." Current Medicinal Chemistry 2, no. 3 (1995): 707–22. http://dx.doi.org/10.2174/092986730203220223144628.

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<P>Adenosine regulates a wide range of physiological functions through specific cell membrane receptors. On the basis of pharmacological studies and molecular cloning, four distinct adenosine receptors have been identified and classified as A1, A2a. A2b and A3. These adenosine receptors are members of the G-protein-coupled receptor family. <P> An intense medicinal chemistry effort made over the last 20 years has led to a variety of selective adenosine receptor agonists and antagonists. While all the agonists thus far identified are related to the adenosine structure, the antagonist

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Cekic, Caglar, Imran Akdemir, Altay Koyas, Merve Kayhan, and Ali Can Savas. "Adenosine regulation of danger signaling." Journal of Immunology 198, no. 1_Supplement (2017): 222.14. http://dx.doi.org/10.4049/jimmunol.198.supp.222.14.

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Abstract Metabolic and immune related activities converge as main triggers of adenosine accumulation in extracellular space. Adenosine by engaging adenosine A2A and A2B receptors strongly suppresses innate and adaptive immune responses. Although adenosine receptors are being targeted in preclinical and clinical studies how different danger signals are regulated by adenosine is poorly understood. Here we showed that adenosine receptor stimulation strongly inhibited inflammatory responses while sparing type-I interferon responses downstream of different danger signals in dendritic cells and macr

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Shin, Hwa Kyoung, Yung Woo Shin, and Ki Whan Hong. "Role of adenosine A2B receptors in vasodilation of rat pial artery and cerebral blood flow autoregulation." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (2000): H339—H344. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h339.

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This study was aimed to investigate the underlying mechanism of vasodilation induced by the activation of A2B adenosine receptors in relation to cerebral blood flow (CBF) autoregulation. Changes in pial arterial diameters were observed directly through a closed cranial window. N ω-nitro-l-arginine methyl ester (l-NAME, nitric oxide synthase inhibitor) significantly suppressed the concentration-dependent vasodilations induced by adenosine and 5′- N-ethylcarboxamido-adenosine (NECA) but not the vasodilation by CGS-21680 (A2A-receptor agonist). Moreover, NECA-induced vasodilation was suppressed b

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Lu, Yan, Rui Zhang, Ying Ge, et al. "Identification and function of adenosine A3 receptor in afferent arterioles." American Journal of Physiology-Renal Physiology 308, no. 9 (2015): F1020—F1025. http://dx.doi.org/10.1152/ajprenal.00422.2014.

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Adenosine plays an important role in regulation of renal microcirculation. All receptors of adenosine, A1, A2A, A2B, and A3, have been found in the kidney. However, little is known about the location and function of the A3 receptor in the kidney. The present study determined the expression and role of A3 receptors in mediating the afferent arteriole (Af-Art) response and studied the interaction of A3 receptors with angiotensin II (ANG II), A1 and A2 receptors on the Af-Art. We found that the A3 receptor expressed in microdissected isolated Af-Art and the mRNA levels of A3 receptor were 59% of

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Jackson, Edwin K., Chongxue Zhu, and Stevan P. Tofovic. "Expression of adenosine receptors in the preglomerular microcirculation." American Journal of Physiology-Renal Physiology 283, no. 1 (2002): F41—F51. http://dx.doi.org/10.1152/ajprenal.00232.2001.

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The purpose of this study was to systematically investigate the abundance of each of the adenosine receptor subtypes in the preglomerular microcirculation vs. other vascular segments and vs. the renal cortex and medulla. Rat preglomerular microvessels (PGMVs) were isolated by iron oxide loading followed by magnetic separation. For comparison, mesenteric microvessels, segments of the aorta (thoracic, middle abdominal, and lower abdominal), renal cortex, and renal medulla were obtained by dissection. Adenosine receptor protein and mRNA expression were examined by Western blotting, Northern blott

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Müller, Christa E. "Tools and Drugs for Purine-Binding Targets—Important Players in Inflammation and Cancer." Proceedings 22, no. 1 (2019): 33. http://dx.doi.org/10.3390/proceedings2019022033.

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Despite decades of research, only few drugs have been approved that interact with purine receptors. Recently, new hypes and hopes have been created in the field, mainly due to the gold rush fever in immuno-oncology. Adenosine is one of the strongest immunosuppressant agents of the innate immune system. Cancer cells and tissues can release large amounts of ATP, which is immediately hydrolyzed by ectonucleotidases. These ecto-enzymes, including ectonucleotide pyrophosphatase/phosphodiesterase 1 (NPP1, CD203a), ectonucleoside diphosphohydrolase 1 (NTPDase1, CD39), and ecto-5′-nucleotidase (CD73)

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Kusano, Yoshikazu, German Echeverry, Greg Miekisiak, et al. "Role of Adenosine A2 Receptors in Regulation of Cerebral Blood Flow during Induced Hypotension." Journal of Cerebral Blood Flow & Metabolism 30, no. 4 (2009): 808–15. http://dx.doi.org/10.1038/jcbfm.2009.244.

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The mechanisms responsible for vascular autoregulation in the brain during changes in mean arterial blood pressure are ambiguous. Potentially, adenosine, a purine nucleoside and potent vasodilator, may be involved as earlier studies have documented an increase in brain adenosine concentrations with cerebral ischemia and hypotension. Consequently, we tested the hypothesis that adenosine is involved in vasodilatation during hypotension within the autoregulatory range (>50 mm Hg) by exposing adenosine 2a receptor (A2aR) knockout and wild type (WT) mice to short (2 to 5 mins) periods of hypoten

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Wang, Lixin, Vasantha Kolachala, Baljit Walia, et al. "Agonist-induced polarized trafficking and surface expression of the adenosine 2b receptor in intestinal epithelial cells: role of SNARE proteins." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 5 (2004): G1100—G1107. http://dx.doi.org/10.1152/ajpgi.00164.2004.

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Adenosine, acting through the A2b receptor, induces vectorial chloride and IL-6 secretion in intestinal epithelia and may play an important role in intestinal inflammation. We have previously shown that apical or basolateral adenosine receptor stimulation results in the recruitment of the A2b receptor to the plasma membrane. In this study, we examined domain specificity of recruitment and the role of soluble N-ethylmaleimide (NEM) attachment receptor (SNARE) proteins in the agonist-mediated recruitment of the A2b receptor to the membrane. The colonic epithelial cell line T84 was used because i

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Shang, Liangcheng, Yaobiao Huang, Xin Xie, Sudan Ye, and Chun Chen. "Effect of Adenosine Receptor Antagonists on Adenosine-Pretreated PC12 Cells Exposed to Paraquat." Dose-Response 20, no. 2 (2022): 155932582210934. http://dx.doi.org/10.1177/15593258221093411.

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Previous studies evaluated the adenosine receptor antagonists alone to determine their effects on oxidative stress, but little is known about adenosine’s protective efficacy when oxidative injury occurs in vivo. Adenosine is a crucial signaling molecule recognized by four distinct G-protein-coupled receptors (GPCRs) (i.e., A1R, A2AR, A2BR, and A3R) and protects cells against pathological conditions. The present study was performed to evaluate the role of antagonist modulation in the setting of paraquat toxicity with adenosine pretreatment. First, PC12 cells were exposed to paraquat (850 μM) an

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Xaus, Jordi, Annabel F. Valledor, Marina Cardó, et al. "Adenosine Inhibits Macrophage Colony-Stimulating Factor-Dependent Proliferation of Macrophages Through the Induction of p27kip-1 Expression." Journal of Immunology 163, no. 8 (1999): 4140–49. http://dx.doi.org/10.4049/jimmunol.163.8.4140.

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Abstract Adenosine is produced during inflammation and modulates different functional activities in macrophages. In murine bone marrow-derived macrophages, adenosine inhibits M-CSF-dependent proliferation with an IC50 of 45 μM. Only specific agonists that can activate A2B adenosine receptors such as 5′-N-ethylcarboxamidoadenosine, but not those active on A1 (N6-(R)-phenylisopropyladenosine), A2A ([p-(2-carbonylethyl)phenylethylamino]-5′-N-ethylcarboxamidoadenosine), or A3 (N6-(3-iodobenzyl)adenosine-5′-N-methyluronamide) receptors, induce the generation of cAMP and modulate macrophage prolifer

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Yu, Weiqun, Lefteris C. Zacharia, Edwin K. Jackson, and Gerard Apodaca. "Adenosine receptor expression and function in bladder uroepithelium." American Journal of Physiology-Cell Physiology 291, no. 2 (2006): C254—C265. http://dx.doi.org/10.1152/ajpcell.00025.2006.

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The uroepithelium of the bladder forms an impermeable barrier that is maintained in part by regulated membrane turnover in the outermost umbrella cell layer. Other than bladder filling, few physiological regulators of this process are known. Western blot analysis established that all four adenosine receptors (A1, A2a, A2b, and A3) are expressed in the uroepithelium. A1 receptors were prominently localized to the apical membrane of the umbrella cell layer, whereas A2a, A2b, and A3 receptors were localized intracellularly or on the basolateral membrane of umbrella cells and the plasma membrane o

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Lindemann, Marcel, Rareş-Petru Moldovan, Sonja Hinz, et al. "Development of a Radiofluorinated Adenosine A2B Receptor Antagonist as Potential Ligand for PET Imaging." International Journal of Molecular Sciences 21, no. 9 (2020): 3197. http://dx.doi.org/10.3390/ijms21093197.

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The adenosine A2B receptor has been proposed as a novel therapeutic target in cancer, as its expression is drastically elevated in several tumors and cancer cells. Noninvasive molecular imaging via positron emission tomography (PET) would allow the in vivo quantification of this receptor in pathological processes and most likely enable the identification and clinical monitoring of respective cancer therapies. On the basis of a bicyclic pyridopyrimidine-2,4-dione core structure, the new adenosine A2B receptor ligand 9 was synthesized, containing a 2-fluoropyridine moiety suitable for labeling w

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