Статті в журналах: "Adenine nucleotides Receptors"

1

Stone, Trevor W. "Receptors for adenosine and adenine nucleotides." General Pharmacology: The Vascular System 22, no. 1 (January 1991): 25–31. http://dx.doi.org/10.1016/0306-3623(91)90305-p.

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2

Newman, George C., Frank E. Hospod, Sean D. Trowbridge, Shilpa Motwani, and Yan Liu. "Restoring Adenine Nucleotides in a Brain Slice Model of Cerebral Reperfusion." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (June 1998): 675–85. http://dx.doi.org/10.1097/00004647-199806000-00010.

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Tissue adenine nucleotides are depleted during cerebral ischemia, impeding recovery after reperfusion. Although prior studies have attempted to prevent the initial loss of adenylates, the present study tests the hypothesis that stimulating synthesis of adenine nucleotides, through either adenosine kinase or adenine phosphoribosyltransferase, would result in significant cerebroprotection. To study the effects on neurons and glia directly while avoiding the influence of the cerebral vasculature, hippocampal brain slices were used for the model of transient ischemia with reperfusion. The standard brain slice insult of brief exposure to anoxia with aglycemia was modified based on studies which showed that a 30-minute exposure to air with 1 mmol/L glucose produced a stable, moderate reduction in ATP during the insult and that, 2 hours after return to normal conditions, there was moderate depletion of tissue adenine nucleotides and histologic injury. Treatments with 1 mmol/L adenosine, AMP, or adenine were equivalent in partially re-storing adenine nucleotides. Despite this, only adenosine af-forded histologic protection, suggesting a protective role for adenosine receptors. There also was evidence for metabolic cycling among adenine nucleotides, nucleosides, and purines. Adenosine may exert direct cerebroprotective effects on neural tissue as well as indirect effects through the cerebral vasculature.

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3

Gorman, Mark W., Kayoko Ogimoto, Margaret V. Savage, Kenneth A. Jacobson, and Eric O. Feigl. "Nucleotide coronary vasodilation in guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H1040—H1047. http://dx.doi.org/10.1152/ajpheart.00981.2002.

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The role of P1 receptors and P2Y1 receptors in coronary vasodilator responses to adenine nucleotides was examined in the isolated guinea pig heart. Bolus arterial injections of nucleotides were made in hearts perfused at constant pressure. Peak increase in flow was measured before and after addition of purinoceptor antagonists. Both the P1 receptor antagonist 8-( p-sulfophenyl)theophylline and adenosine deaminase inhibited adenosine vasodilation. AMP-induced vasodilation was inhibited by P1 receptor blockade but not by adenosine deaminase or by the selective P2Y1 antagonist N6-methyl-2′-deoxyadenosine 3′,5′-bisphosphate (MRS 2179). ADP-induced vasodilation was moderately inhibited by P1 receptor blockade and greatly inhibited by combined P1 and P2Y1 blockade. ATP-induced vasodilation was antagonized by P1 blockade but not by adenosine deaminase. Addition of P2Y1 blockade to P1 blockade shifted the ATP dose-response curve further rightward. It is concluded that in this preparation ATP-induced vasodilation results primarily from AMP stimulation of P1 receptors, with a smaller component from ATP or ADP acting on P2Y1 receptors. ADP-induced vasodilation is largely due to P2Y1 receptors, with a smaller contribution by AMP or adenosine acting via P1 receptors. AMP responses are mediated solely by P1 receptors. Adenosine contributes very little to vasodilation resulting from bolus intracoronary injections of ATP, ADP, or AMP.

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4

Murugappan, Swaminathan, Haripriya Shankar, and Satya P. Kunapuli. "Platelet Receptors for Adenine Nucleotides and Thromboxane A2." Seminars in Thrombosis and Hemostasis 30, no. 4 (August 2004): 411–18. http://dx.doi.org/10.1055/s-2004-833476.

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5

Eltzschig, Holger K., Linda F. Thompson, Jorn Karhausen, Richard J. Cotta, Juan C. Ibla, Simon C. Robson, and Sean P. Colgan. "Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism." Blood 104, no. 13 (December 15, 2004): 3986–92. http://dx.doi.org/10.1182/blood-2004-06-2066.

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Abstract Hypoxia is a well-documented inflammatory stimulus and results in tissue polymorphonuclear leukocyte (PMN) accumulation. Likewise, increased tissue adenosine levels are commonly associated with hypoxia, and given the anti-inflammatory properties of adenosine, we hypothesized that adenosine production via adenine nucleotide metabolism at the vascular surface triggers an endogenous anti-inflammatory response during hypoxia. Initial in vitro studies indicated that endogenously generated adenosine, through activation of PMN adenosine A2A and A2B receptors, functions as an antiadhesive signal for PMN binding to microvascular endothelia. Intravascular nucleotides released by inflammatory cells undergo phosphohydrolysis via hypoxia-induced CD39 ectoapyrase (CD39 converts adenosine triphosphate/adenosine diphosphate [ATP/ADP] to adenosine monophosphate [AMP]) and CD73 ecto-5′-nucleotidase (CD73 converts AMP to adenosine). Extensions of our in vitro findings using cd39- and cd73-null animals revealed that extracellular adenosine produced through adenine nucleotide metabolism during hypoxia is a potent anti-inflammatory signal for PMNs in vivo. These findings identify CD39 and CD73 as critical control points for endogenous adenosine generation and implicate this pathway as an innate mechanism to attenuate excessive tissue PMN accumulation. (Blood. 2004;104:3986-3992)

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6

Williams, Wynford R. "Dampening of neurotransmitter action: molecular similarity within the melatonin structure." Endocrine Regulations 52, no. 4 (October 1, 2018): 199–207. http://dx.doi.org/10.2478/enr-2018-0025.

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AbstractObjectives. Melatonin initiates physiologic and therapeutic responses in various tissues through binding to poorly defined MT receptors regulated by G-proteins and purine nucleotides. Melatonin’s interaction with other G-protein regulated receptors, including those of serotonin, is unclear. This study explores the potential for the interaction of melatonin with nucleotide and receptor ligand structures. Methods. The study uses a computational program to investigate relative molecular similarity by the comparative superimposition and quantitative fitting of molecular structures to adenine and guanine nucleotide templates. Results. A minimum energy melatonin conformer replicates the nucleotide fits of ligand structures that regulate Gαi and Gαq proteins via serotonin, dopamine, opioid, α-adrenoceptor, and muscarinic receptor classes. The same conformer also replicates the nucleotide fits of ligand structures regulating K+ and Ca2+ ion channels. The acyl-methoxy distance within the melatonin conformer matches a carbonyl-hydroxyl distance in guanine nucleotide. Conclusion. Molecular similarity within the melatonin and ligand structures relates to the established effects of melatonin on cell receptors regulated by purine nucleotides in cell signal transduction processes. Pharmacologic receptor promiscuity may contribute to the widespread effects of melatonin.

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7

Antos, Laura K., and Lincoln R. Potter. "Adenine nucleotides decrease the apparentKmof endogenous natriuretic peptide receptors for GTP." American Journal of Physiology-Endocrinology and Metabolism 293, no. 6 (December 2007): E1756—E1763. http://dx.doi.org/10.1152/ajpendo.00321.2007.

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Natriuretic peptide receptors A (NPR-A) and B (NPR-B) mediate most effects of natriuretic peptides by synthesizing cGMP. ATP increases the activity of these receptors by an unknown mechanism. We recently reported that a nonhydrolyzable form of ATP, adenylyl imidodiphosphate (AMPPNP), stabilizes but is not required for the activation of NPR-A and NPR-B in membranes from highly overexpressing cells. Here, we repeated these studies on receptors expressed in endogenous settings. Kinetic analysis indicated that both AMPPNP and ATP dramatically decrease the apparent Kmof both receptors for GTP but had little effect on the Vmax. The EC50for AMPPNP decreased as substrate concentration increased whereas the magnitude of the effect was greater at lower GTP concentrations. ATP increased the activity of a mutant receptor containing glutamates substituted for all known phosphorylation sites similarly to the wild-type receptor, consistent with a phosphorylation independent mechanism. Finally, the putative ATP binding sites were investigated. Mutation of the ATP modulatory domain region had no effect, but mutation of K535A dramatically diminished ANP-dependent cyclase activity in a manner that was unresponsive to ATP. Mutation of the highly conserved 630-KSS to AAA (all alanines) resulted in an expressed receptor that had no detectable guanylyl cyclase activity. We conclude that ATP is not required for the initial activation of NPRs but does increase activity over time by reducing the apparent Kmfor GTP.

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8

Kawa, Kazuyoshi. "Discrete but simultaneous release of adenine nucleotides and serotonin from mouse megakaryocytes as detected with patch- and carbon-fiber electrodes." American Journal of Physiology-Cell Physiology 286, no. 1 (January 2004): C119—C128. http://dx.doi.org/10.1152/ajpcell.00014.2003.

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Using patch- and carbon-fiber electrodes, we studied release phenomena of adenine nucleotides and serotonin from megakaryocytes isolated from the bone marrow of the mouse. Megakaryocytes express ionotropic purinergic receptors on their surfaces. Under the condition of whole cell recording, the cells showed spikelike spontaneous inward currents. The spontaneous currents were carried by cations and had amplitudes of 30–800 pA at –43 mV and durations of 0.1–0.3 s. Pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS; 100 μM) and suramin (100 μM), purinoceptor-blocking agents, depressed the currents reversibly. It is thought that the receptor involved was the P2X1 subtype on the cell and that the currents were due to activation of the P2X1 receptor by adenine nucleotides released from the cell. The currents showed a skewed amplitude distribution, suggesting variation of vesicular contents and/or distinct localization or varied density of receptors on the cell. Frequency of the spontaneous inward currents was enhanced by external application of platelet-activating substances, thrombin (0.4 U/ml), phorbol ester (100 nM), and ADP (2 μM), at low concentrations. With a carbon-fiber electrode, which can detect oxidizable substances including serotonin, spikelike oxidation currents from the external surface of the megakaryocyte were detected. The frequency of the oxidation currents increased remarkably after the application of thrombin (10 U/ml). The majority of the oxidation currents coincided with the rising phase of the whole cell currents, suggesting corelease of serotonin and adenine nucleotide from the same vesicle. We concluded that megakaryocytes store adenine nucleotides and serotonin in the same vesicle and release them simultaneously in a discrete manner.

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9

Puchałowicz, Kamila, Maciej Tarnowski, Marta Tkacz, Dariusz Chlubek, Patrycja Kłos, and Violetta Dziedziejko. "Extracellular Adenine Nucleotides and Adenosine Modulate the Growth and Survival of THP-1 Leukemia Cells." International Journal of Molecular Sciences 21, no. 12 (June 22, 2020): 4425. http://dx.doi.org/10.3390/ijms21124425.

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A new approach to improve the effectiveness of acute myeloid leukemia (AML) treatment is to use the properties of purinergic signaling molecules secreted into the bone marrow milieu in response to leukemic cell growth. Therefore, our study aimed to evaluate the effects of extracellular adenine nucleotides and adenosine on the growth and death parameters in the leukemic THP-1 cell line. Cells were exposed to ATP, ADP, AMP, adenosine and nonhydrolyzable analogues of ATP and ADP (ATPγS and ADPβS) in a 1–1000 μM broad concentration range. The basal mRNA expression of the P1 and P2 receptors was evaluated by real-time PCR. Changes in the processes of cell growth and death were assessed by flow cytometry analysis of proliferation, cell cycle and apoptosis. Chemotaxis toward stromal cell-derived factor-1 (SDF-1) was performed using the modified Boyden chamber assay, and chemokine receptor type 4 (CXCR4) surface expression was quantified by flow cytometry. We indicated several antileukemic actions. High micromolar concentrations (100–1000 μM) of extracellular adenine nucleotides and adenosine inhibit the growth of cells by arresting the cell cycle and/or inducing apoptosis. ATP is characterized by the highest potency and widest range of effects, and is responsible for the cell cycle arrest and the apoptosis induction. Compared to ATP, the effect of ADP is slightly weaker. Adenosine mostly has a cytotoxic effect, with the induction of apoptosis. The last studied nucleotide, AMP, demonstrated only a weak cytotoxic effect without affecting the cell cycle. In addition, cell migration towards SDF-1 was inhibited by low micromolar concentrations (10 μM). One of the reasons for this action of ATPγS and adenosine was a reduction in CXCR4 surface expression, but this only partially explains the mechanism of antimigratory action. In summary, extracellular adenine nucleotides and adenosine inhibit THP-1 cell growth, cause death of cells and modulate the functioning of the SDF-1/CXCR4 axis. Thus, they negatively affect the processes that are responsible for the progression of AML and the difficulties in AML treatment.

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10

Cattaneo, M. "The platelet P2 receptors in inflammation." Hämostaseologie 35, no. 03 (2015): 262–66. http://dx.doi.org/10.5482/hamo-14-09-0044.

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SummaryIn addition to their well characterized and established role in haemostasis and thrombosis, platelets contribute to the pathogenesis of inflammation. Adenine nucleotides are signalling molecules that regulate the function of virtually every cell in the body, by interacting with P2 receptors. Their important role in inflammation is well established. In the last few years, the pro-inflammatory roles of adenine nucleotides interacting with their platelet P2 receptors has emerged. In particular, it was shown that the platelet P2Y12 receptor for ADP significantly contributed to the proinflammatory effects of cysteinyl leukotrienes (CysLT) in experimental models of asthma in mice. More importantly, it was recently shown that P2Y12 variants were associated with lung function in a large family-based asthma cohort and that the P2Y12 antagonist prasugrel tended to decrease bronchial hyper-reactivity to mannitol in patients with allergic bronchial asthma in a randomized, placebo controlled trial.These data strongly suggest that P2Y12 may represent an important pharmacological target for the treatment of patients with allergic bronchial asthma.

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11

Guzman-Aranguez, Ana, Xavier Gasull, Yolanda Diebold, and Jesús Pintor. "Purinergic Receptors in Ocular Inflammation." Mediators of Inflammation 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/320906.

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Inflammation is a complex process that implies the interaction between cells and molecular mediators, which, when not properly “tuned,” can lead to disease. When inflammation affects the eye, it can produce severe disorders affecting the superficial and internal parts of the visual organ. The nucleoside adenosine and nucleotides including adenine mononucleotides like ADP and ATP and dinucleotides such as P1,P4-diadenosine tetraphosphate (Ap4A), and P1,P5-diadenosine pentaphosphate (Ap5A) are present in different ocular locations and therefore they may contribute/modulate inflammatory processes. Adenosine receptors, in particularA2Aadenosine receptors, present anti-inflammatory action in acute and chronic retinal inflammation. Regarding the A3receptor, selective agonists like N6-(3-iodobenzyl)-5′-N-methylcarboxamidoadenosine (CF101) have been used for the treatment of inflammatory ophthalmic diseases such as dry eye and uveoretinitis. Sideways, diverse stimuli (sensory stimulation, large intraocular pressure increases) can produce a release of ATP from ocular sensory innervation or after injury to ocular tissues. Then, ATP will activate purinergic P2 receptors present in sensory nerve endings, the iris, the ciliary body, or other tissues surrounding the anterior chamber of the eye to produce uveitis/endophthalmitis. In summary, adenosine and nucleotides can activate receptors in ocular structures susceptible to suffer from inflammatory processes. This involvement suggests the possible use of purinergic agonists and antagonists as therapeutic targets for ocular inflammation.

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12

REES, D. Aled, Maurice F. SCANLON, and Jack HAM. "Novel insights into how purines regulate pituitary cell function." Clinical Science 104, no. 5 (May 1, 2003): 467–81. http://dx.doi.org/10.1042/cs20030053.

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Purine nucleosides and nucleotides are widely distributed substances that exhibit a diverse range of effects in a number of tissues, acting as important extracellular signalling molecules in addition to their more established roles in cellular metabolism. They mediate their effects via activation of distinct cell surface receptors, termed adenosine (or P1) and P2 purinergic receptors. Although roles for adenosine and adenine nucleotides have been described previously in the pituitary gland, the distribution of the receptor subtypes and the effects of their activation on pituitary function are not well defined. Recent evidence, however, has emerged to describe a complex signalling system for purines in the pituitary gland. Data from a variety of studies have shown that the expression pattern, number and affinity of adenosine and/or P2 receptors may be cell-type specific and that non-endocrine in addition to endocrine cells elaborate these receptors. These variations, along with the diverse range of signalling pathways activated, dictate the response of individual cell types to extracellular purines, with roles now emerging for these substances in the regulation of hormone release, pituitary cell proliferation and cytokine/growth factor expression. In this review, we discuss these advances and examine some implications for pituitary growth control and the response of the hypothalamic–pituitary–adrenal axis to stress and inflammation.

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13

Reddington, M. "Interactions of adenine nucleotides with A1 receptors in rat brain membranes." Japanese Journal of Pharmacology 52 (1990): 92. http://dx.doi.org/10.1016/s0021-5198(19)32966-x.

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14

Biffen, M., and D. R. Alexander. "Mobilization of intracellular Ca2+ by adenine nucleotides in human T-leukaemia cells: evidence for ADP-specific and P2y-purinergic receptors." Biochemical Journal 304, no. 3 (December 15, 1994): 769–74. http://dx.doi.org/10.1042/bj3040769.

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The expression of purinergic receptors on human T-cells was investigated and the receptors were shown to be functionally coupled to intracellular signals in two out of eight T-leukaemia cell-lines. Addition of adenine nucleotides resulted in mobilization of intracellular Ca2+ in HPB-ALL cells and a cell line (CB1) recently isolated from a patient with T-acute lymphoblastic leukaemia. Of a range of nucleotides tested only ADP and ATP elevated intracellular levels of Ca2+, with ADP being the more potent agonist. Ca2+ mobilization by ATP was accompanied by increased inositol phosphate production and was blocked by the purinergic receptor antagonist, Reactive Blue 2, indicating that ATP was interacting with a P2y receptor. Intracellular Ca2+ release triggered by ADP was independent of both inositol phosphate production and protein tyrosine phosphorylation. Expression of the transmembrane phosphotyrosine phosphatase, CD45, had no effect on ADP-stimulated Ca2+ mobilization. Our results show that functional P2y receptors can be expressed on T-cells, and also identify a novel T-cell ADP receptor. Signals mediated by these purinergic receptors could play important roles in modulating T-cell function.

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15

Nemeth, E. F., and L. M. Kosz. "Adenine nucleotides mobilize cellular Ca2+ and inhibit parathyroid hormone secretion." American Journal of Physiology-Endocrinology and Metabolism 257, no. 4 (October 1, 1989): E505—E513. http://dx.doi.org/10.1152/ajpendo.1989.257.4.e505.

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Measurements of the concentration of intracellular free calcium [( Ca2+]i) were used to screen for the presence of Ca2+-mobilizing receptors on dissociated and purified bovine parathyroid cells loaded with fura-2. Among a wide variety of agents known to mobilize cellular Ca2+ in other cells, only ATP and certain other nucleotides were capable of altering [Ca2+]i in parathyroid cells. The addition of ATP or adenosine 5'-O-(3-thiotriphosphate) (ATP gamma S) (10-200 microM) to parathyroid cells evoked a rapid and transient increase that was followed by a small, steady-state increase in [Ca2+]i. Cytosolic Ca2+ transients elicited by ATP or ATP gamma S persisted in the absence of extracellular Ca2+ and presence of a mitochondrial uncoupler but were blocked by pretreatment with ionomycin or fluoride. Cytosolic Ca2+ transients elicited by ATP were inhibited by increased concentrations of extracellular Ca2+, Mg2+, or Sr2+. Conversely, ATP depressed increases in [Ca2+]i elicited by these extracellular divalent cations. Parathyroid hormone (PTH) secretion was inhibited by ATP gamma S but not by those nucleotides that were without effect on [Ca2+]i. Loading cells with 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid and fura-2 blocked cytosolic Ca2+ transients elicited by ATP gamma S but did not block the inhibitory effects of ATP gamma S on PTH secretion. The results show that the activation of a calcium-mobilizing receptor, in this case by ATP gamma S, is sufficient to inhibit PTH secretion. This favors the view that extracellular Ca2+ acts via a Ca2+-mobilizing receptor to regulate PTH secretion.

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16

Borowiec, Agnieszka, Katarzyna Lechward, Kinga Tkacz-Stachowska, and Andrzej C. Składanowski. "Adenosine as a metabolic regulator of tissue function: production of adenosine by cytoplasmic 5'-nucleotidases." Acta Biochimica Polonica 53, no. 2 (June 12, 2006): 269–78. http://dx.doi.org/10.18388/abp.2006_3339.

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Adenosine is a product of complete dephosphorylation of adenine nucleotides which takes place in various compartments of the cell. This nucleoside is a significant signal molecule engaged in regulation of physiology and modulation of the function of numerous cell types (i.e. neurons, platelets, neutrophils, mast cells and smooth muscle cells in bronchi and vasculature, myocytes etc.). As part a of purinergic signaling system, adenosine mediates neurotransmission, conduction, secretion, vasodilation, proliferation and cell death. Most of the effects of adenosine help to protect cells and tissues during stress conditions such as ischemia or anoxia. Adenosine receptors and nucleoside transporters are targets for potential drugs in many pathophysiological situations. The adenosine-producing system in vertebrates involves a cascade dephosphorylating ATP and ending with 5'-nucleotidase (EC 3.1.3.5) localized either on the membrane or inside the cell. In this paper the cytoplasmic variants of 5'-nucleotidase are broadly characterized as well as their clinical relevance. The role of AMP-selective 5'-nucleotidase (cN-I) in the heart, skeletal muscle and brain is highlighted. cN-I action is crucial during ischemia and important for the efficacy of some nucleoside-based drugs and in the regulation of the substrate pool for nucleic acids synthesis. Inhibitors used in studying the roles of cytoplasmic and membrane-bound 5'-nucleotidases are also described.

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17

Schicker, Klaus, Simon Hussl, Giri K. Chandaka, Kristina Kosenburger, Jae-Won Yang, Maria Waldhoer, Harald H. Sitte, and Stefan Boehm. "A membrane network of receptors and enzymes for adenine nucleotides and nucleosides." BMC Pharmacology 8, Suppl 1 (2008): A40. http://dx.doi.org/10.1186/1471-2210-8-s1-a40.

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18

Schicker, Klaus, Simon Hussl, Giri K. Chandaka, Kristina Kosenburger, Jae-Won Yang, Maria Waldhoer, Harald H. Sitte, and Stefan Boehm. "A membrane network of receptors and enzymes for adenine nucleotides and nucleosides." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1793, no. 2 (February 2009): 325–34. http://dx.doi.org/10.1016/j.bbamcr.2008.09.014.

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19

Buxton, D. B., S. M. Robertson, and M. S. Olson. "Stimulation of glycogenolysis by adenine nucleotides in the perfused rat liver." Biochemical Journal 237, no. 3 (August 1, 1986): 773–80. http://dx.doi.org/10.1042/bj2370773.

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Infusion of adenine nucleotides and adenosine into perfused rat livers resulted in stimulation of hepatic glycogenolysis, transient increases in the effluent perfusate [3-hydroxybutyrate]/[acetoacetate] ratio, and increased portal vein pressure. In livers perfused with buffer containing 50 microM-Ca2+, transient efflux of Ca2+ was seen on stimulation of the liver with adenine nucleotides or adenosine. ADP was the most potent of the nucleotides, stimulating glucose output at concentrations as low as 0.15 microM, with half-maximal stimulation at approx. 1 microM, and ATP was slightly less potent, half-maximal stimulation requiring 4 microM-ATP. AMP and adenosine were much less effective, doses giving half-maximal stimulation being 40 and 20 microM respectively. Non-hydrolysed ATP analogues were much less effective than ATP in promoting changes in hepatic metabolism. ITP, GTP and GDP caused similar changes in hepatic metabolism to ATP, but were 10-20 times less potent than ATP. In livers perfused at low (7 microM) Ca2+, infusion of phenylephrine before ATP desensitized hepatic responses to ATP. Repeated infusions of ATP in such low-Ca2+-perfused livers caused homologous desensitization of ATP responses, and also desensitized subsequent Ca2+-dependent responses to phenylephrine. A short infusion of Ca2+ (1.25 mM) after phenylephrine infusion restored subsequent responses to ATP, indicating that, during perfusion with buffer containing 7 microM-Ca2+, ATP and phenylephrine deplete the same pool of intracellular Ca2+, which can be rapidly replenished in the presence of extracellular Ca2+. Measurement of cyclic AMP in freeze-clamped liver tissue demonstrated that adenosine (150 microM) significantly increased hepatic cyclic AMP, whereas ATP (15 microM) was without effect. It is concluded that ATP and ADP stimulate hepatic glycogenolysis via P2-purinergic receptors, through a Ca2+-dependent mechanism similar to that in alpha-adrenergic stimulation of hepatic tissue. However, adenosine stimulates glycogenolysis via P1-purinoreceptors and/or uptake into the cell, at least partially through a mechanism involving increase in cyclic AMP. Further, the hepatic response to adenine nucleotides may be significant in regulating hepatic glucose output in physiological and pathophysiological states.

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20

Mannix, R. J., T. Moatter, K. A. Kelley, and M. E. Gerritsen. "Cellular signaling responses mediated by a novel nucleotide receptor in rabbit microvessel endothelium." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H675—H680. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h675.

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The adenine nucleotide, ATP, elicits an elevation in intracellular ionized calcium concentration ([Ca2+]i) and phospholipase C-mediated phosphatidylinositol hydrolysis and stimulates the synthesis of the prostaglandins E2 and I2 in cultured endothelial cells derived from rabbit cardiac muscle. Use of various ATP analogues indicated that these events did not fit the classical definition of P1 or P2 purinergic receptors and, furthermore, indicated that the receptor(s) mediating these activities was not specific for purines. The rank order of agonist potency on prostaglandin release, elevations in [Ca2+]i, and inositol phosphate response was UTP > or = ATP > ADP > ADP[beta]S = 2-methylthio ATP > adenosine, suggesting that these three cellular responses are coupled to the same or similar receptors. However, the sensitivity of these three cellular responses to added nucleotides was somewhat different. The half-maximum effective concentration (EC50) for ATP stimulation of prostaglandin release was 100 microM, for inositol phosphate turnover it was 25 microM, and for elevations in [Ca2+]i it was < 1 microM. Similar discrepancies in EC50 UTP values for these three cellular responses were also noted. These observations indicate that purine and pyrimidine nucleotides elicit at least three cellular responses in rabbit cardiac muscle microvessel endothelial cells, all demonstrating similar rank orders of potency. However, the differences in EC50 suggest that if these responses are mediated by a single receptor type, it exhibits divergent coupling to various cellular signaling pathways.

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21

LEMMENS, Raf, Luc VANDUFFEL, Henri TEUCHY, and Ognjen CULIC. "Regulation of proliferation of LLC-MK2 cells by nucleosides and nucleotides: the role of ecto-enzymes." Biochemical Journal 316, no. 2 (June 1, 1996): 551–57. http://dx.doi.org/10.1042/bj3160551.

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1. Using the incorporation of [methyl-3H]thymidine as a proliferation marker, the effects of various nucleosides and nucleotides on endothelial LLC-MK2 cells were studied. We found that ATP, ADP, AMP and adenosine in concentrations of 10 μM or higher stimulate the proliferation of these cells. 2. Inhibition of ecto-ATPase (EC 3.6.1.15), 5´-nucleotidase (EC 3.1.3.5) or alkaline phosphatase (EC 3.1.3.1) significantly diminished the stimulatory effect of ATP, indicating that the effect is primarily caused by adenosine and not by adenine nucleotides. Also, the effect depends only on extracellular nucleosides, since inhibition of nucleoside uptake by dipyridamole has no influence on proliferation. 3. Other purine nucleotides and nucleosides (ITP, GTP, inosine and guanosine) also stimulate cell proliferation, while pyrimidine nucleotides and nucleosides (CTP, UTP, cytidine and uridine) inhibit proliferation. Furthermore, the simultaneous presence of adenosine and any of the other purine nucleosides is not entirely additive in its effect on cell proliferation. At the same time any pyrimidine nucleoside, when added together with adenosine, has the same inhibitory effect as the pyrimidine nucleoside alone. 4. Apparently these proliferative effects are neither caused by any pharmacologically known P1-purinoceptor, nor are they mediated by cyclic AMP, cyclic GMP, or D-myo-inositol 1,4,5-trisphosphate as second messenger, nor by extracellular Ca2+. 5. Therefore, we conclude that various purine and pyrimidine nucleosides can influence the proliferation of LLC-MK2 cells by acting on putative purinergic and pyrimidinergic receptors not previously described.

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22

Salter, Kelli D., J. Gregory Fitz, and Richard M. Roman. "Domain-specific purinergic signaling in polarized rat cholangiocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 3 (March 1, 2000): G492—G500. http://dx.doi.org/10.1152/ajpgi.2000.278.3.g492.

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In cholangiocytes, adenine nucleotides function as autocrine/paracrine signals that modulate ductular ion transport by activation of purinergic receptors. The purpose of these studies was to identify cellular signals that modulate ATP release and nucleotide processing in polarized normal rat cholangiocytes. In Ussing chamber studies, selective exposure of the apical and basolateral membranes to ATP or adenosine 5′- O-(3-thiotriphosphate) (ATPγS) stimulated increases in short-circuit current. Apical purinergic receptor agonist preference was consistent with the P2Y2subtype. In contrast, basolateral ADP was more potent in stimulating transepithelial currents, consistent with the expression of different basolateral P2 receptor(s). Luminometric analysis revealed that both membranes exhibited constitutive ATP efflux. Hypotonic exposure enhanced ATP release in both compartments, whereas decreases in ATP efflux during hypertonicity were more prominent at the apical membrane. Increases in intracellular cAMP, cGMP, and Ca2+ also increased ATP permeability, but selective effects on apical and basolateral ATP release differed. Finally, the kinetics of ATP degradation in apical and basolateral compartments were distinct. These findings suggest that there are domain-specific signaling pathways that contribute to purinergic responses in polarized cholangiocytes.

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23

Cote, S., J. Van Sande, and J. M. Boeynaems. "Enhancement of endothelial cAMP accumulation by adenine nucleotides: role of methylxanthine-sensitive sites." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (May 1, 1993): H1498—H1503. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1498.

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ATP is a well-known inducer of prostacyclin and nitric oxide release from vascular endothelial cells. These responses are mediated by P2 receptors coupled to a phospholipase C. We have investigated the influence of ATP on the control of adenosine 3',5'-cyclic monophosphate (cAMP) in bovine aortic endothelial cells. ATP produced a slight increase in the cAMP content of unstimulated endothelial cells. A more impressive response to ATP (5-fold) was observed in forskolin-stimulated cells. The rank orders of potency of various ATP analogues were strikingly different for the increase in cAMP and the accumulation of inositol phosphates. The action of ATP was unaffected by indomethacin. Protein kinase C downregulation produced only a partial inhibition of the ATP response. The effect of phorbol 12-myristate 13-acetate and bradykinin on the forskolin-induced accumulation of cAMP was much smaller than that of ATP. Neither adenosine deaminase nor AMP deaminase decreased the response to ATP, which thus cannot result from the ATP degradation into adenosine. However, 8-(p-sulfophenyl)theophylline inhibited the responses to both ATP and adenosine. In conclusion, ATP enhances the accumulation of cAMP in endothelial cells. This action appears to be the sum of two components: a minor one resulting from kinase C activation and a major one mediated either by a direct interaction of ATP with A2 receptors, or by putative methylxanthine-sensitive P2 receptors.

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Kasztan, Małgorzata, Agnieszka Piwkowska, Ewelina Kreft, Dorota Rogacka, Irena Audzeyenka, Mirosława Szczepanska-Konkel, and Maciej Jankowski. "Extracellular purines' action on glomerular albumin permeability in isolated rat glomeruli: insights into the pathogenesis of albuminuria." American Journal of Physiology-Renal Physiology 311, no. 1 (July 1, 2016): F103—F111. http://dx.doi.org/10.1152/ajprenal.00567.2015.

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Purinoceptors (adrengeric receptors and P2 receptors) are expressed on the cellular components of the glomerular filtration barrier, and their activation may affect glomerular permeability to albumin, which may ultimately lead to albuminuria, a well-established risk factor for the progression of chronic kidney disease and development of cardiovascular diseases. We investigated the mechanisms underlying the in vitro and in vivo purinergic actions on glomerular filter permeability to albumin by measuring convectional albumin permeability ( Palb) in a single isolated rat glomerulus based on the video microscopy method. Primary cultured rat podocytes were used for the analysis of Palb, cGMP accumulation, PKG-Iα dimerization, and immunofluorescence. In vitro, natural nucleotides (ATP, ADP, UTP, and UDP) and nonmetabolized ATP analogs (2-meSATP and ATP-γ-S) increased Palb in a time- and concentration-dependent manner. The effects were dependent on P2 receptor activation, nitric oxide synthase, and cytoplasmic guanylate cyclase. ATP analogs significantly increased Palb, cGMP accumulation, and subcortical actin reorganization in a PKG-dependent but nondimer-mediated route in cultured podocytes. In vivo, 2-meSATP and ATP-γ-S increased Palb but did not significantly affect urinary albumin excretion. Both agonists enhanced the clathrin-mediated endocytosis of albumin in podocytes. A product of adenine nucleotides hydrolysis, adenosine, increased the permeability of the glomerular barrier via adrenergic receptors in a dependent and independent manner. Our results suggest that the extracellular nucleotides that stimulate an increase of glomerular Palb involve nitric oxide synthase and cytoplasmic guanylate cyclase with actin reorganization in podocytes.

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Park, Hyung Seo, Matthew J. Betzenhauser, Yu Zhang, and David I. Yule. "Regulation of Ca2+ release through inositol 1,4,5-trisphosphate receptors by adenine nucleotides in parotid acinar cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 1 (January 2012): G97—G104. http://dx.doi.org/10.1152/ajpgi.00328.2011.

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Secretagogue-stimulated intracellular Ca2+ signals are fundamentally important for initiating the secretion of the fluid and ion component of saliva from parotid acinar cells. The Ca2+ signals have characteristic spatial and temporal characteristics, which are defined by the specific properties of Ca2+ release mediated by inositol 1,4,5-trisphosphate receptors (InsP3R). In this study we have investigated the role of adenine nucleotides in modulating Ca2+ release in mouse parotid acinar cells. In permeabilized cells, the Ca2+ release rate induced by submaximal [InsP3] was increased by 5 mM ATP. Enhanced Ca2+ release was not observed at saturating [InsP3]. The EC50 for the augmented Ca2+ release was ∼8 μM ATP. The effect was mimicked by nonhydrolysable ATP analogs. ADP and AMP also potentiated Ca2+ release but were less potent than ATP. In acini isolated from InsP3R-2-null transgenic animals, the rate of Ca2+ release was decreased under all conditions but now enhanced by ATP at all [InsP3]. In addition the EC50 for ATP potentiation increased to ∼500 μM. These characteristics are consistent with the properties of the InsP3R-2 dominating the overall features of InsP3R-induced Ca2+ release despite the expression of all isoforms. Finally, Ca2+ signals were measured in intact parotid lobules by multiphoton microscopy. Consistent with the release data, carbachol-stimulated Ca2+ signals were reduced in lobules exposed to experimental hypoxia compared with control lobules only at submaximal concentrations. Adenine nucleotide modulation of InsP3R in parotid acinar cells likely contributes to the properties of Ca2+ signals in physiological and pathological conditions.

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26

El-Moatassim, Chakib, Nicole Bernad, Jean-Claude Mani, and Jacques Dornand. "Extracellular ATP induces a nonspecific permeability of thymocyte plasma membranes." Biochemistry and Cell Biology 67, no. 9 (September 1, 1989): 495–502. http://dx.doi.org/10.1139/o89-080.

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We have previously demonstrated that extracellular ATP can give medullary thymocytes the calcium message required for the induction of their blastogenesis, without mobilization of intracellular calcium. We describe here the effects of extracellular nucleotides on membrane permeability to monovalent and divalent cations in mouse thymocytes. Among all nucleotides tested, under physiological conditions, only ATP and, to a lesser extent, 2-methylthio-ATP, adenosine 5′-O-(3-thio-triphosphate), and ADP were able to depolarize thymocyte plasma membranes and to induce Na+ and Ca2+ influxes into thymocytes; other nonhydrolysable ATP analogs were only effective in the absence of Mg2+. The ATP-induced effects were inhibited in a dose-dependent manner by Mg2+ and greatly potentiated in its absence, which suggests that the tetrabasic ATP4− is probably the active species and that a phosphotransferase activity is not involved in its effects. These ATP-mediated changes in ion fluxes result from an increase in nonspecific permeability of thymocyte membranes, probably by pore formation. These ion flux changes might be responsible for the mitogenic induction of phorbol 12-myristate 13-acetate treated medullary thymocytes. The potency order for the adenine derivatives to affect these fluxes (ATP>ADP> >AMP>adenosine) suggests the presence of ATP specific receptors (P2 purinergic receptors) on thymocyte plasma membranes.Key words: purinergic receptors, extracellular ATP, membrane potential, cation fluxes, thymocytes.

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27

Dal Ben, D., M. Buccioni, C. Lambertucci, G. Marucci, R. Volpini, and G. Cristalli. "The Importance of Alkynyl Chain Presence for the Activity of Adenine Nucleosides/Nucleotides on Purinergic Receptors." Current Medicinal Chemistry 18, no. 10 (April 1, 2011): 1444–63. http://dx.doi.org/10.2174/092986711795328391.

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28

Fuentes-Martínez, Juan P., Diana Gutiérrez-Rodríguez, Edgar Rogel García, Karla I. Rivera-Márquez, Felipe Medrano, Oscar Torres-Ángeles, Evelin Castillo-Vargas, Blanca E. Duque Montaño, and Carolina Godoy-Alcántar. "Streptomycin Hydrazone Derivatives: Synthesis and Molecular Recognition in Aqueous Solution." Natural Product Communications 9, no. 10 (October 2014): 1934578X1400901. http://dx.doi.org/10.1177/1934578x1400901012.

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Five hydrazone derivatives of streptomycin were synthetized (D0h, D1ph, D2bt, D3dctf, D4ag) and characterized by IR, 1H and 13C NMR spectroscopy, mass spectrometry and elemental analysis. Protonation constants were determined by potentiometry for all derivatives. D1ph and D2bt derivatives were investigated as receptors of dicarboxylates and adenine nucleotides in aqueous solution by potentiometric and 1H NMR titrations. D1ph and D2bt derivatives have the highest affinity with AMP and ATP, respectively, which shows that electrostatic forces are not always the dominant factor in binding of streptomycin derivatives with nucleotides, but the conformational fit between them. Calculated structures at the DFT level of the D1ph derivative bonded with either AMP or ADP showed that the complexes are stabilized by the formation of multiple interactions with the receptors. The antibiotic activity of the derivatives was explored and compared with native streptomycin.

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29

Zhang, Xuejun, Jiayu Wen, Keshore R. Bidasee, Henry R. Besch, and Ronald P. Rubin. "Ryanodine receptor expression is associated with intracellular Ca2+ release in rat parotid acinar cells." American Journal of Physiology-Cell Physiology 273, no. 4 (October 1, 1997): C1306—C1314. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1306.

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The ryanodine receptor mediates intracellular Ca2+ mobilization in muscle and nerve, but its physiological role in nonexcitable cells is less well defined. Like adenosine 3′,5′-cyclic monophosphate and inositol 1,4,5-trisphosphate, cyclic ADP-ribose (0.3–5 μM) and ADP (1–25 μM) produced a concentration-dependent rise in cytosolic Ca2+ in permeabilized rat parotid acinar cells. Adenosine and AMP were less effective. Ryanodine markedly depressed the Ca2+-mobilizing action of the adenine nucleotides and forskolin in permeabilized cells and was likewise effective in depressing the action of forskolin in intact cells. Cyclic ADP-ribose-evoked Ca2+ release was enhanced by calmodulin and depressed by W-7, a calmodulin inhibitor. A fluorescently labeled ligand, 4,4-difluoro-1,3,5,7-tetramethyl-4-bora-3,4-diaza-s-indacene-3-propionic acid-glycyl ryanodine, was synthesized to detect the expression and distribution of ryanodine receptors. In addition, ryanodine receptor expression was detected in rat parotid cells with a sequence highly homologous to a rat skeletal muscle type 1 and a novel brain type 1 ryanodine receptor. These findings demonstrate the presence of a ryanodine-sensitive intracellular Ca2+ store in rat parotid cells that shares many of the characteristics of stores in muscle and nerve and may mediate Ca2+-induced Ca2+ release or a modified form of this process.

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30

Ninomiya, Hideki, Hajime Otani, Kejie Lu, Takamichi Uchiyama, Masakuni Kido, and Hiroji Imamura. "Complementary role of extracellular ATP and adenosine in ischemic preconditioning in the rat heart." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 5 (May 1, 2002): H1810—H1820. http://dx.doi.org/10.1152/ajpheart.00760.2001.

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Although adenosine is an important mediator of ischemic preconditioning (IPC), its relative contribution to IPC remains unknown. Because adenosine is formed through the hydrolysis of ATP, the present study investigated the role of ATP and adenosine in IPC. Isolated and buffer-perfused rat hearts underwent IPC by three cycles of 5-min ischemia and 5-min reperfusion before 25 min of global ischemia. The rate-pressure product (RPP) 30 min after reperfusion was taken as an endpoint of functional protection. Interstitial fluid (ISF) adenine nucleotides and adenosine were measured by cardiac microdialysis techniques. Inhibition of IPC-induced recovery of RPP was partial by the adenosine receptor antagonist 8-( p-sulfophenyl)theophylline (SPT; 100 μM) or by the structurally distinct P2Y purinoceptor antagonists suramin (300 μM) or reactive blue (RB; 10 μM) but was additive when SPT was given with suramin or RB. The P2X antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid tetrasodium (50 μM) had no effect on functional protection. The improved functional recovery was not significantly affected by an ecto-5′-nucleotidase inhibitor, α,β-methylene adenosine diphosphate (AMP-CP; 100 μM), alone but was inhibited by AMP-CP plus SPT, suramin, or RB. ISF ATP and adenosine increased temporarily by 10-fold during IPC. AMP-CP augmented the increase in ISF ATP associated with the decrease in ISF adenosine. There was a reciprocal correlation between the ISF concentration of ATP and adenosine in preconditioned hearts. In addition, there was a significant correlation between ISF adenosine and ATP and the inhibitory potency of SPT and suramin or RB against functional protection conferred by IPC. These results suggest that extracellular ATP and adenosine play a complementary role in IPC through P2Y purinoceptors and adenosine receptors, respectively.

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31

Vasconcellos, CA, and SE Lind. "Coordinated inhibition of actin-induced platelet aggregation by plasma gelsolin and vitamin D-binding protein." Blood 82, no. 12 (December 15, 1993): 3648–57. http://dx.doi.org/10.1182/blood.v82.12.3648.3648.

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Abstract Actin is an abundant intracellular protein that is released into the blood during tissue injury and its injection into rats causes microthrombi to form in the vasculature. This report and others have shown that actin filaments are able to aggregate platelets in an adenosine diphosphate (ADP)-dependent manner. The effects on this process of two plasma actin-binding proteins, vitamin D-binding protein (DBP) and gelsolin, were examined separately and together. The addition of DBP, a monomer-binding protein, to actin filaments did not affect their ability to induce platelet aggregation. However, severing of actin filaments with gelsolin resulted in an increased degree of platelet aggregation. Preincubation of F-actin with both gelsolin and DBP resulted in a significant inhibition of aggregation. The effects of DBP and gelsolin on actin-induced aggregation paralleled their effects on exchange of actin-bound adenine nucleotides. DBP inhibited 1, N6- ethenoadenosine 5′ triphosphate (epsilon-ATP) exchange with G-actin but not with F-actin. Gelsolin increased epsilon-ATP exchange with F-actin, which was largely abrogated by the addition of DBP. These results suggest that gelsolin's severing (and subsequent capping) of actin filaments not only results in an increase in the number of pointed filament ends but also in the dissociation of actin monomers containing ADP. Phalloidin, which stabilizes actin filaments while decreasing both monomer and nucleotide exchange, inhibited actin-induced aggregation, as well, indicating that depolymerization of actin filaments is not required to inhibit aggregation. Platelet activation by either G- or F- actin may thus be regulated by the local concentrations of the plasma actin-binding proteins gelsolin and DBP. Together, these proteins inhibit platelet aggregation in a manner that can be explained by their effects on actin's filament structure and the accessibility of its bound ADP. Depletion of DBP or gelsolin may allow actin released from injured tissues to stimulate purinergic receptors on platelets, and perhaps other cells, via its bound adenine nucleotides.

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32

Vasconcellos, CA, and SE Lind. "Coordinated inhibition of actin-induced platelet aggregation by plasma gelsolin and vitamin D-binding protein." Blood 82, no. 12 (December 15, 1993): 3648–57. http://dx.doi.org/10.1182/blood.v82.12.3648.bloodjournal82123648.

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Анотація:

Actin is an abundant intracellular protein that is released into the blood during tissue injury and its injection into rats causes microthrombi to form in the vasculature. This report and others have shown that actin filaments are able to aggregate platelets in an adenosine diphosphate (ADP)-dependent manner. The effects on this process of two plasma actin-binding proteins, vitamin D-binding protein (DBP) and gelsolin, were examined separately and together. The addition of DBP, a monomer-binding protein, to actin filaments did not affect their ability to induce platelet aggregation. However, severing of actin filaments with gelsolin resulted in an increased degree of platelet aggregation. Preincubation of F-actin with both gelsolin and DBP resulted in a significant inhibition of aggregation. The effects of DBP and gelsolin on actin-induced aggregation paralleled their effects on exchange of actin-bound adenine nucleotides. DBP inhibited 1, N6- ethenoadenosine 5′ triphosphate (epsilon-ATP) exchange with G-actin but not with F-actin. Gelsolin increased epsilon-ATP exchange with F-actin, which was largely abrogated by the addition of DBP. These results suggest that gelsolin's severing (and subsequent capping) of actin filaments not only results in an increase in the number of pointed filament ends but also in the dissociation of actin monomers containing ADP. Phalloidin, which stabilizes actin filaments while decreasing both monomer and nucleotide exchange, inhibited actin-induced aggregation, as well, indicating that depolymerization of actin filaments is not required to inhibit aggregation. Platelet activation by either G- or F- actin may thus be regulated by the local concentrations of the plasma actin-binding proteins gelsolin and DBP. Together, these proteins inhibit platelet aggregation in a manner that can be explained by their effects on actin's filament structure and the accessibility of its bound ADP. Depletion of DBP or gelsolin may allow actin released from injured tissues to stimulate purinergic receptors on platelets, and perhaps other cells, via its bound adenine nucleotides.

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33

Bagatini, Margarete Dulce, Alessandra Antunes dos Santos, Andréia Machado Cardoso, Aline Mânica, Cristina Ruedell Reschke, and Fabiano Barbosa Carvalho. "The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases." Journal of Immunology Research 2018 (August 12, 2018): 1–21. http://dx.doi.org/10.1155/2018/4892473.

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Evidences show that purinergic signaling is involved in processes associated with health and disease, including noncommunicable, neurological, and degenerative diseases. These diseases strike from children to elderly and are generally characterized by progressive deterioration of cells, eventually leading to tissue or organ degeneration. These pathological conditions can be associated with disturbance in the signaling mediated by nucleotides and nucleosides of adenine, in expression or activity of extracellular ectonucleotidases and in activation of P2X and P2Y receptors. Among the best known of these diseases are atherosclerosis, hypertension, cancer, epilepsy, Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). The currently available treatments present limited effectiveness and are mostly palliative. This review aims to present the role of purinergic signaling highlighting the ectonucleotidases E-NTPDase, E-NPP, E-5′-nucleotidase, and adenosine deaminase in noncommunicable, neurological, and degenerative diseases associated with the cardiovascular and central nervous systems and cancer. In conclusion, changes in the activity of ectonucleotidases were verified in all reviewed diseases. Although the role of ectonucleotidases still remains to be further investigated, evidences reviewed here can contribute to a better understanding of the molecular mechanisms of highly complex diseases, which majorly impact on patients’ quality of life.

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Guarracino, Juan F., Alejandro R. Cinalli, Verónica Fernández, Liliana I. Roquel, and Adriana S. Losavio. "P2Y 13 receptors mediate presynaptic inhibition of acetylcholine release induced by adenine nucleotides at the mouse neuromuscular junction." Neuroscience 326 (June 2016): 31–44. http://dx.doi.org/10.1016/j.neuroscience.2016.03.066.

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35

Cunha, Rodrigo A., Paulo Correia-de-Sá, Ana M. Sebastião, and J. Alexandre Ribeiro. "Preferential activation of excitatory adenosine receptors at rat hippocampal and neuromuscular synapses by adenosine formed from released adenine nucleotides." British Journal of Pharmacology 119, no. 2 (September 1996): 253–60. http://dx.doi.org/10.1111/j.1476-5381.1996.tb15979.x.

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36

Song, L., SM Carter, Y. Chen, and R. Sitsapesan. "Diadenosine pentaphosphate is a potent activator of cardiac ryanodine receptors revealing a novel high-affinity binding site for adenine nucleotides." British Journal of Pharmacology 156, no. 5 (March 26, 2009): 857–67. http://dx.doi.org/10.1111/j.1476-5381.2008.00071.x.

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37

von Kügelgen, Ivar, Leni Späth, and Klaus Starke. "Stable adenine nucleotides inhibit [3H]-noradrenaline release in rabbit brain cortex slices by direct action at presynaptic adenosine A1-receptors." Naunyn-Schmiedeberg's Archives of Pharmacology 346, no. 2 (August 1992): 187–96. http://dx.doi.org/10.1007/bf00165300.

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38

Hung, C. T., F. D. Allen, K. D. Mansfield, and I. M. Shapiro. "Extracellular ATP modulates [Ca2+]i in retinoic acid-treated embryonic chondrocytes." American Journal of Physiology-Cell Physiology 272, no. 5 (May 1, 1997): C1611—C1617. http://dx.doi.org/10.1152/ajpcell.1997.272.5.c1611.

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When treated with low doses of retinoic acid (RA), cephalic chondrocytes of the chick embryonic sternum mature and express phenotypic characteristics of postmitotic hypertrophic cells. In concert with these maturation-dependent changes, cells release adenine nucleotides into the culture medium. To ascertain if these compounds modulate chondrocyte function, we challenged chondrocytes with nucleotides and measured one determinant of the signal transduction pathway, intracellular Ca2+ concentration ([Ca2+]i). In the presence of micromolar concentrations of ATP, there was a dose-dependent elevation in chondrocyte [Ca2+]i; ADP caused a small but significant rise in the peak [Ca2+]i response. We found that the change in the [Ca2+]i response is linked to retinoid-dependent maturation of chondrocytes. Thus the [Ca2+]i rise was dependent on the RA concentration and treatment time. Immature caudal chondrocytes, cells that were not affected by RA, were used as control cells for this study. When treated with ATP, these cells did not exhibit a [Ca2+]i response. Although the purinergic subtype receptor was not characterized, the observation that cells responded to ATP and ADP but were refractory to AMP and adenosine suggested that P2 purinoceptors were expressed by chondrocytes. Because, during the same culture period, chondrocytes exhibited many of the unique characteristics of the terminally differentiated cell, the acquisition of purinergic receptors represents a new feature associated with expression of the mature phenotype. Finally, to ascertain if the ATP-dependent response was due to release of Ca2+ from intracellular stores, cells were treated with thapsigargin. Since this compound significantly reduced the [Ca2+]i signal, we concluded that the ATP response is mediated by release of cation, from the endoplasmic reticulum.

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39

Murayama, Takashi, Nagomi Kurebayashi, and Yasuo Ogawa. "Role of Mg2+ in Ca2+-Induced Ca2+ Release through Ryanodine Receptors of Frog Skeletal Muscle: Modulations by Adenine Nucleotides and Caffeine." Biophysical Journal 78, no. 4 (April 2000): 1810–24. http://dx.doi.org/10.1016/s0006-3495(00)76731-2.

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40

Marteau, Frédéric, Didier Communi, Jean-Marie Boeynaems, and Nathalie Suarez Gonzalez. "Involvement of multiple P2Y receptors and signaling pathways in the action of adenine nucleotides diphosphates on human monocyte-derived dendritic cells." Journal of Leukocyte Biology 76, no. 4 (July 7, 2004): 796–803. http://dx.doi.org/10.1189/jlb.0104032.

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41

Weiss, Harvey, and Bruce Lages. "Secreted Dense Granule Adenine Nucleotides Promote Calcium Influx and the Maintenance of Elevated Cytosolic Calcium Levels in Stimulated Human Platelets." Thrombosis and Haemostasis 81, no. 02 (1999): 286–92. http://dx.doi.org/10.1055/s-0037-1614459.

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SummaryEvidence that secreted dense granule adenine nucleotides mediate part of the agonist-induced cytosolic calcium ([Ca2+]i) responses in human platelets was obtained from comparisons of fura-2-loaded platelets from normal subjects and from patients with a form of platelet storage pool deficiency (SPD) in which the secretory dense granules and their contents are virtually absent. SPD platelets had normal initial [Ca2+]i in creases induced by thrombin and the endoperoxide analog U46619, but a significantly enhanced decay of elevated [Ca2+]i levels following the initial increases. With thrombin, this enhanced [Ca2+]i decay was associated with decreased Ca2+ influx, as measured by Mn2+ quench of fura-2 fluorescence. Addition of micromolar concentrations of ADP, alone or together with ATP, after stimulation reversed the enhanced [Ca2+]I decay and increased Mn2+ quench in SPD platelets, but had no effect on these responses in normal platelets, while addition of 100-fold higher concentrations of ATP or apyrase before stimulation increased [Ca2+]I decay and decreased Mn2+ quench in normal platelets, but had little effect in SPD platelets. ATP and α,β-methylene ATP, a specific agonist for P2X1 receptors, at micromolar concentrations also increased Mn2+ quench, but to lesser extents than did ADP, in SPD platelets isolated and loaded with fura-2 in the presence of apyrase. Similar effects of ADP and excess ATP were seen in U46619-stimulated platelets, but decreased Ca2+ influx could not be measured directly in SPD platelets, presumably due to the very transient influx response seen with U46619. These results suggest that secreted dense granule ADP and ATP contribute to the maintenance of elevated [Ca2+]i levels, but not to the initial [Ca2+]i increases, in stimulated human platelets, most likely via a nucleotide-specific component of Ca2+ influx which may be mediated by interactions with both P2X1 and P2Y1 purinoceptors.

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42

Santos, Karen Freitas, Jessié Martins Gutierres, Micheli Mainardi Pillat, Vitor Braga Rissi, Maria do Carmo dos Santos Araújo, Gustavo Bertol, Paulo Bayard Dias Gonçalves, Maria Rosa Chitolina Schetinger, and Vera Maria Morsch. "Uncaria tomentosa extract alters the catabolism of adenine nucleotides and expression of ecto-5′-nucleotidase/CD73 and P2X7 and A1 receptors in the MDA-MB-231 cell line." Journal of Ethnopharmacology 194 (December 2016): 108–16. http://dx.doi.org/10.1016/j.jep.2016.08.051.

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43

Laubinger, Werner, and Georg Reiser. "Differential characterization of binding sites for adenine and uridine nucleotides in membranes from rat lung as possible tools for studying P2 receptors in lung." Biochemical Pharmacology 55, no. 5 (March 1998): 687–95. http://dx.doi.org/10.1016/s0006-2952(97)00532-7.

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44

Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (June 1, 1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.bloodjournal6761568.

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A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule secretion was impaired. The ultrastructural appearance of thrombopathic platelets was normal. Fibrinogen-platelet interaction was evaluated by reacting platelet-rich plasma (PRP) with fibrinogen coupled to polymeric acrylonitrile beads and scoring the extent of stimulus-induced agglutination. The aggregatory responses of normal and thrombopathic platelets were closely correlated with fibrinogen receptor availability. In contrast to human platelets, epinephrine-stimulated canine platelets did not interact with immobilized fibrinogen, and arachidonate generally induced only weak agglutination. Thrombopathic platelets agglutinated fibrinogen beads at reduced rates when stimulated with physiologic doses of thrombin and high-dose calcium ionophore, A23187. Our data suggest that thrombin-mediated induction of canine platelet fibrinogen receptors may proceed by pathway(s) alternate to those shared by other platelet agonists, and/or that secreted granule constituents may act synergistically with thrombin to overcome inhibition of signal-response- coupled reactions mediating the interaction of fibrinogen with its receptor. This congenital platelet defect provides further evidence, in a species other than human, for the pivotal role of fibrinogen receptor induction in platelet aggregation.

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45

Chari, R. S., S. M. Schutz, J. E. Haebig, G. H. Shimokura, P. B. Cotton, J. G. Fitz, and W. C. Meyers. "Adenosine nucleotides in bile." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (February 1, 1996): G246—G252. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g246.

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Activation of purinergic receptors by ATP stimulates Cl- efflux in biliary epithelial cells. To determine whether purinergic agonists are present under physiological conditions, we have assayed mammalian bile for nucleotides and assessed whether hepatoma and cholangiocarcinoma cell lines are capable of nucleotide release. Bile samples were collected from human, rat, and pig donors and assayed for nucleotide concentrations by luminometry. ATP, ADP, and AMP were present in bile from each species, and the average total nucleotide concentration in human bile was 5.21 +/- 0.91 microM (n = 16). In an in vitro model of HTC rat hepatoma cells or Mz-ChA-1 cholangiocarcinoma cells on a superfused column, nucleotides were present in the effluent from each cell type. Addition of alpha, beta-methyleneadenosine 5'-diphosphate (50 microM) to inhibit 5'-nucleotidase activity increased AMP concentrations two- to threefold. Exposure to forskolin (100 microM) or ionomycin (2 microM) stimulated nucleotide release from cholangiocarcinoma but not hepatoma cells. These studies indicate that adenosine nucleotides are present in bile in concentrations sufficient to activate purinergic receptors. Purinergic receptor activation by local nucleotide release might constitute an autocrine and/or paracrine mechanism for modulation of biliary secretion.

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46

Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (June 1, 1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.1568.

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Abstract A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule secretion was impaired. The ultrastructural appearance of thrombopathic platelets was normal. Fibrinogen-platelet interaction was evaluated by reacting platelet-rich plasma (PRP) with fibrinogen coupled to polymeric acrylonitrile beads and scoring the extent of stimulus-induced agglutination. The aggregatory responses of normal and thrombopathic platelets were closely correlated with fibrinogen receptor availability. In contrast to human platelets, epinephrine-stimulated canine platelets did not interact with immobilized fibrinogen, and arachidonate generally induced only weak agglutination. Thrombopathic platelets agglutinated fibrinogen beads at reduced rates when stimulated with physiologic doses of thrombin and high-dose calcium ionophore, A23187. Our data suggest that thrombin-mediated induction of canine platelet fibrinogen receptors may proceed by pathway(s) alternate to those shared by other platelet agonists, and/or that secreted granule constituents may act synergistically with thrombin to overcome inhibition of signal-response- coupled reactions mediating the interaction of fibrinogen with its receptor. This congenital platelet defect provides further evidence, in a species other than human, for the pivotal role of fibrinogen receptor induction in platelet aggregation.

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47

Kawashima, Yasuko, Toshiro Nagasawa, and Haruhiko Ninomiya. "Contribution of ecto-5′-nucleotidase to the inhibition of platelet aggregation by human endothelial cells." Blood 96, no. 6 (September 15, 2000): 2157–62. http://dx.doi.org/10.1182/blood.v96.6.2157.

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Abstract We studied the role of adenosine (Ado), which is generated from adenine nucleotides via the activity of ecto-5′-nucleotidase (ecto-5′-NT), in the inhibition of platelet aggregation by endothelial cells (ECs). The enzymatic activity of nucleotidases on human umbilical vein endothelial cells (HUVECs) was examined with regard to (1) the inhibition of adenosine diphosphate (ADP)–induced platelet aggregation and (2) the liberation of inorganic phosphate from adenine nucleotides. Adenosine 5′-monophosphate (AMP) preincubated with HUVECs significantly inhibited ADP-induced platelet aggregation. This was completely blocked by the treatment of HUVECs with a specific inhibitor of ecto-5′-NT, 5′-[αβ-methylene] diphosphate (APCP), or by the addition of an A2a receptor antagonist. Neither nitric oxide nor prostacyclin was involved in this inhibitory activity, suggesting that Ado generated in the incubation medium by the activity of 5′-NT on HUVECs inhibited platelet aggregation. When ADP was incubated on HUVECs, it lost most of its agonistic activity for platelets. Pretreatment of HUVECs with APCP at a concentration that abolished ecto-5′-NT activity partially restored ADP-induced platelet aggregation. Ecto-5′-NT contributes to EC function by inhibiting platelet aggregation in cooperation with ATP diphosphohydrolase, which degrades ADP to AMP.

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48

Kawashima, Yasuko, Toshiro Nagasawa, and Haruhiko Ninomiya. "Contribution of ecto-5′-nucleotidase to the inhibition of platelet aggregation by human endothelial cells." Blood 96, no. 6 (September 15, 2000): 2157–62. http://dx.doi.org/10.1182/blood.v96.6.2157.h8002157_2157_2162.

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We studied the role of adenosine (Ado), which is generated from adenine nucleotides via the activity of ecto-5′-nucleotidase (ecto-5′-NT), in the inhibition of platelet aggregation by endothelial cells (ECs). The enzymatic activity of nucleotidases on human umbilical vein endothelial cells (HUVECs) was examined with regard to (1) the inhibition of adenosine diphosphate (ADP)–induced platelet aggregation and (2) the liberation of inorganic phosphate from adenine nucleotides. Adenosine 5′-monophosphate (AMP) preincubated with HUVECs significantly inhibited ADP-induced platelet aggregation. This was completely blocked by the treatment of HUVECs with a specific inhibitor of ecto-5′-NT, 5′-[αβ-methylene] diphosphate (APCP), or by the addition of an A2a receptor antagonist. Neither nitric oxide nor prostacyclin was involved in this inhibitory activity, suggesting that Ado generated in the incubation medium by the activity of 5′-NT on HUVECs inhibited platelet aggregation. When ADP was incubated on HUVECs, it lost most of its agonistic activity for platelets. Pretreatment of HUVECs with APCP at a concentration that abolished ecto-5′-NT activity partially restored ADP-induced platelet aggregation. Ecto-5′-NT contributes to EC function by inhibiting platelet aggregation in cooperation with ATP diphosphohydrolase, which degrades ADP to AMP.

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49

Okajima, F., H. Tomura, and Y. Kondo. "Enkephalin activates the phospholipase C/Ca2+ system through cross-talk between opioid receptors and P2-purinergic or bradykinin receptors in NG 108–15 cells. A permissive role for pertussis toxin-sensitive G-proteins." Biochemical Journal 290, no. 1 (February 15, 1993): 241–47. http://dx.doi.org/10.1042/bj2900241.

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In an NG 108-15 neuroblastoma x glioma hybrid cell suspension, extracellular ATP (via P2-purinergic receptors) and bradykinin stimulated Ins(1,4,5)P3 formation, which was accompanied by an increase in the cytosolic Ca2+ concentration ([Ca2+]i). Leucine enkephalin (EK) also slightly increased [Ca2+]i in the absence, but not in the presence, of apyrase, which hydrolyses extracellular ATP and ADP to AMP. When the cells were stimulated by P2-agonists or bradykinin prior to the application of EK, EK induces a remarkable rise in [Ca2+]i. This P2-agonist- or bradykinin-assisted EK action was also observed in single cells on a coverslip. A decrease in the extracellular Ca2+ concentration only slightly lowered the EK-induced rise in [Ca2+]i, but treatment of the cells with thapsigargin, an agent which depletes Ca2+ in the Ins(1,4,5)P3-sensitive pool, almost completely abolished EK action. The observed permissive stimulation by EK of Ins(1,4,5)P3 formation induced by a P2-agonist or bradykinin may be a primary event for the EK-induced [Ca2+]i rise. These actions of EK were antagonized by naloxone and completely reversed by prior treatment of the cells with pertussis toxin, whereas the toxin hardly affected the actions of P2-agonists and bradykinin themselves. Thus EK can induce phospholipase C activation and subsequent Ca2+ mobilization, provided that the cells have been previously or are simultaneously stimulated by endogenous adenine nucleotides or by externally applied P2-agonists or bradykinin. In this cross-talk mechanism between opioid receptors and these Ca(2+)-mobilizing agonist receptors, pertussis toxin-sensitive G-proteins play a permissive role.

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50

MISSIAEN, Ludwig, Jan B. PARYS, Humbert DE SMEDT, Ilse SIENAERT, Henk SIPMA, Sara VANLINGEN, Karlien MAES, and Rik CASTEELS. "Effect of adenine nucleotides on myo-inositol-1,4,5-trisphosphate-induced calcium release." Biochemical Journal 325, no. 3 (August 1, 1997): 661–66. http://dx.doi.org/10.1042/bj3250661.

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The effects of a whole series of adenine nucleotides on Ins(1,4,5)P3-induced Ca2+ release were characterized in permeabilized A7r5 smooth-muscle cells. Several adenine nucleotides activated the Ins(1,4,5)P3 receptor. It was observed that 3′-phosphoadenosine 5′-phosphosulphate, CoA, di(adenosine-5′)tetraphosphate (Ap4A) and di(adenosine-5′)pentaphosphate (Ap5A) were more effective than ATP. Ap4A and Ap5A also interacted with a lower EC50 than ATP. In order to find out how these adenine nucleotides affected Ins(1,4,5)P3-induced Ca2+ release, we have measured their effect on the response of permeabilized A7r5 cells to a progressively increasing Ins(1,4,5)P3 concentration. Stimulatory ATP and Ap5A concentrations had no effect on the threshold Ins(1,4,5)P3 concentration for initiating Ca2+ release, but they stimulated Ca2+ release in the presence of supra-threshold Ins(1,4,5)P3 concentrations by increasing the co-operativity of the release process. Inhibition of the Ins(1,4,5)P3-induced Ca2+ release at higher ATP concentrations was associated with a further increase in co-operativity and also with a shift in threshold towards higher Ins(1,4,5)P3 concentrations. ATP had no effect on the non-specific Ca2+ leak in the absence of Ins(1,4,5)P3. We conclude that the adenine-nucleotide-binding site can be activated by many different adenine nucleotides. Binding of these compounds to the transducing domain of the Ins(1,4,5)P3 receptor increases the efficiency of transmitting Ins(1,4,5)P3 binding to channel opening. The inhibition by high ATP concentrations is exerted at a different site, related to Ins(1,4,5)P3 binding.

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