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Journal articles on the topic 'Adenosine diphosphate; ADP; Blood'

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Published: 4 June 2021

Last updated: 17 February 2022

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1

Poelstra, K., JF Baller, MJ Hardonk, and WW Bakker. "Demonstration of antithrombotic activity of glomerular adenosine diphosphatase [published erratum appears in Blood 1991 Oct 15;78(8):2163]." Blood 78, no. 1 (1991): 141–48. http://dx.doi.org/10.1182/blood.v78.1.141.bloodjournal781141.

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We have demonstrated that reduced glomerular adenosine diphosphatase (ADPase) activity within the rat kidney is associated with an increased thrombotic tendency. To establish a possible causal relationship between these intraglomerular events, experiments were conducted to inhibit adenosine diphosphate (ADP) degradation without influencing other glomerular prothrombotic or antithrombotic mechanisms. Concurrently, we studied intraglomerular platelet aggregation. Two ways of selective inhibition of glomerular ADPase activity were applied: (1) by competitive substrates (ie, uridine diphosphate [U

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Poelstra, K., JF Baller, MJ Hardonk, and WW Bakker. "Demonstration of antithrombotic activity of glomerular adenosine diphosphatase [published erratum appears in Blood 1991 Oct 15;78(8):2163]." Blood 78, no. 1 (1991): 141–48. http://dx.doi.org/10.1182/blood.v78.1.141.141.

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Abstract We have demonstrated that reduced glomerular adenosine diphosphatase (ADPase) activity within the rat kidney is associated with an increased thrombotic tendency. To establish a possible causal relationship between these intraglomerular events, experiments were conducted to inhibit adenosine diphosphate (ADP) degradation without influencing other glomerular prothrombotic or antithrombotic mechanisms. Concurrently, we studied intraglomerular platelet aggregation. Two ways of selective inhibition of glomerular ADPase activity were applied: (1) by competitive substrates (ie, uridine dipho

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3

Cattaneo, Marco, Christian Gachet, Jeanne-Pierre Cazenave, and Marian A. Packham. "Adenosine diphosphate (ADP) does not induce thromboxane A2 generation in human platelets." Blood 99, no. 10 (2002): 3868–70. http://dx.doi.org/10.1182/blood-2002-01-0313.

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4

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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Cattaneo, Marco. "The platelet P2Y12 receptor for adenosine diphosphate: congenital and drug-induced defects." Blood 117, no. 7 (2011): 2102–12. http://dx.doi.org/10.1182/blood-2010-08-263111.

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Abstract P2Y12, the Gi-coupled platelet receptor for adenosine diphosphate (ADP), plays a central role in platelet function. Patients with congenital P2Y12 defects display a mild to moderate bleeding diathesis, characterized by mucocutaneous bleedings and excessive post-surgical and post-traumatic blood loss. Defects of P2Y12 should be suspected when ADP, even at high concentrations (≥ 10μM), is unable to induce full, irreversible platelet aggregation. Tests that evaluate the degree of inhibition of adenylyl cyclase by ADP should be used to confirm the diagnosis. Drugs that inhibit P2Y12 are p

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6

Goto, Shinya, Noriko Tamura, and Shunnosuke Handa. "Effects of adenosine 5′-diphosphate (ADP) receptor blockade on platelet aggregation under flow." Blood 99, no. 12 (2002): 4644–46. http://dx.doi.org/10.1182/blood-2001-12-0284.

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7

Muhsin, A., M. T. Eusni Raha, M. N. Sabariah, A. K. Faraizah, H. Roshida, and M. S. Salmiah. "Impaired Platelet Aggregation to Adenosine Diphosphate (ADP) Agonist in National Blood Centre, Malaysia." Asian Journal of Epidemiology 5, no. 4 (2012): 114–22. http://dx.doi.org/10.3923/aje.2012.114.122.

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8

Koessler, Juergen, Philipp Klingler, Marius Niklaus, et al. "The Impact of Cold Storage on Adenosine Diphosphate-Mediated Platelet Responsiveness." TH Open 04, no. 03 (2020): e163-e172. http://dx.doi.org/10.1055/s-0040-1714254.

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Abstract Introduction Cold storage of platelets is considered to contribute to lower risk of bacterial growth and to more efficient hemostatic capacity. For the optimization of storage strategies, it is required to further elucidate the influence of refrigeration on platelet integrity. This study focused on adenosine diphosphate (ADP)-related platelet responsiveness. Materials and Methods Platelets were prepared from apheresis-derived platelet concentrates or from peripheral whole blood, stored either at room temperature or at 4°C. ADP-induced aggregation was tested with light transmission. Ac

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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.505.

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Abstract The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-se

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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.bloodjournal822505.

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The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-selectin ex

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11

Gachet, Christian, and Beatrice Hechler. "Platelet Purinergic Receptors in Thrombosis and Inflammation." Hämostaseologie 40, no. 02 (2020): 145–52. http://dx.doi.org/10.1055/a-1113-0711.

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AbstractIt took approximately 40 years from the seminal identification of adenosine diphosphate (ADP) as the factor R, an agent derived from red blood cells inducing platelet adhesion to glass, to the completion of the repertoire of its receptors on platelets and its importance in haemostasis and thrombosis. ADP, either derived from red blood cells or released by platelets themselves, stimulates platelets via two G protein-coupled receptors, P2Y1 and P2Y12. In addition, adenosine triphosphate, also contained in the platelet dense granules, activates the P2X1 cation channel. Each of these recep

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12

Kim, Phyo, James D. Jones, and Thoralf M. Sundt. "High-energy phosphate levels in the cerebral artery during chronic vasospasm after subarachnoid hemorrhage." Journal of Neurosurgery 76, no. 6 (1992): 991–96. http://dx.doi.org/10.3171/jns.1992.76.6.0991.

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✓ High-energy phosphate levels were measured in the canine cerebral artery during chronic vasospasm. Subarachnoid hemorrhage and vasospasm were induced by percutaneous injections of autologous venous blood into the cisterna magna. Narrowing of the artery was confirmed by angiography 7 days later. Levels of adenosine phosphates (adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP)), guanosine phosphates (guanosine triphosphate (GTP) and guanosine diphosphate (GDP)), and creatine phosphate (CrP) in the basilar artery were quantified using high-performance

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Vial, Catherine, Samantha J. Pitt, Jon Roberts, Michael G. Rolf, Martyn P. Mahaut-Smith, and Richard J. Evans. "Lack of evidence for functional ADP-activated human P2X1 receptors supports a role for ATP during hemostasis and thrombosis." Blood 102, no. 10 (2003): 3646–51. http://dx.doi.org/10.1182/blood-2003-06-1963.

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AbstractPurine nucleotides acting through P2 receptors play key roles in platelet signaling. The P2X1 receptor is an adenosine triphosphate (ATP)-gated ion channel that mediates a rapid calcium influx signal, but can also synergize with subsequent adenosine diphosphate (ADP)-evoked P2Y1 receptor-mediated responses and thus may contribute to platelet activation during hemostasis. Recent studies have shown that P2X1 receptors contribute to the formation of platelet thrombi, particularly under conditions of high shear stress. Based on intracellular Ca2+ measurements a previous report has suggeste

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14

Kajita, Yasukazu, Hans H. Dietrich, and Ralph G. Dacey. "Effects of oxyhemoglobin on local and propagated vasodilatory responses induced by adenosine, adenosine diphosphate, and adenosine triphosphate in rat cerebral arterioles." Journal of Neurosurgery 85, no. 5 (1996): 908–16. http://dx.doi.org/10.3171/jns.1996.85.5.0908.

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✓ After subarachnoid hemorrhage (SAH), cerebral arteries display impaired vasomotor control, resulting in decreased regional cerebral blood flow. Recently, propagation of vasomotor responses has been recognized as an important regulatory mechanism in microcirculation. In this study, the authors tested the hypothesis that oxyhemoglobin (OxyHb) inhibits the vasodilatory effect of chemical mediators such as adenosine and adenine nucleotides at a local and/or propagated site. Penetrating intracerebral arterioles were surgically isolated from the middle cerebral arteries of rat brains, cannulated,

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15

Eltzschig, Holger K., Linda F. Thompson, Jorn Karhausen, et al. "Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism." Blood 104, no. 13 (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 sig

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Cho, Moon J., Junling Liu, Tamara I. Pestina та ін. "The roles of αIIbβ3-mediated outside-in signal transduction, thromboxane A2, and adenosine diphosphate in collagen-induced platelet aggregation". Blood 101, № 7 (2003): 2646–51. http://dx.doi.org/10.1182/blood-2002-05-1363.

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Collagen-induced activation of platelets in suspension leads to αIIbβ3-mediated outside-in signaling, granule release, thromboxane A2 (TxA2) production, and aggregation. Although much is known about collagen-induced platelet signaling, the roles of TxA2 production, adenosine diphosphate (ADP) and dense-granule secretion, and αIIbβ3-mediated outside-in signaling in this process are unclear. Here, we demonstrate that TxA2 and ADP are required for collagen-induced platelet activation in response to a low, but not a high, level of collagen and that αIIbβ3-mediated outside-in signaling is required,

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17

Benedikter, Hermann, Gisela Knopki, and Paul Renz. "Phosphatidylinositol-Specific Phospholipase C from Bovine Blood Platelets. Inhibition by Calmodulin-Inhibitors — Activation by ATP and ADP." Zeitschrift für Naturforschung C 40, no. 1-2 (1985): 68–72. http://dx.doi.org/10.1515/znc-1985-1-214.

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The phospholipase C-activity in crude extracts of bovine blood platelets is strongly inhibited by the calmodulin-inhibitors fluphenazine and calmidazolium in the mᴍ range, and activated by ATP and ADP. but not by AMP. The activating effect is also shown by the nonhydrolysable ATP- and ADP-analogs α,β- and β,γ-methyleneadenosine 5′-triphosphate and α,β-methylene- adenosine 5′-diphosphate, thus indicating that it is an allosteric effect. The stimulation of the phospholipase C-activity by ATP is also detectable in some partially purified fractions of the crude platelet extract, but it is abolishe

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18

Nagaoka, S., H. Shinbara, M. Okubo, T. Kawakita, K. Hino, and E. Sumiya. "Contributions of Adp and Atp to the Increase in Skeletal Muscle Blood Flow after Manual Acupuncture Stimulation in Rats." Acupuncture in Medicine 34, no. 3 (2016): 229–34. http://dx.doi.org/10.1136/acupmed-2015-010959.

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Objective To investigate the contributions of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) to the increase in skeletal muscle blood flow (MBF) observed following manual acupuncture (MA) stimulation in rats. Methods Male Sprague-Dawley rats were used as experimental animals (300–370 g, n=40). MA was applied to the right tibialis anterior muscle (TA) for 1 min using a stainless steel acupuncture needle. In eight rats, high-performance liquid chromatography with the microdialysis technique was used to measure local extracellular concentrations of ATP, ADP, adenosine monophosphate

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19

Sukeksi, Andri, and Rizqi Yogania Rahmawati. "Potensi Ekstrak Etanol Daun Sirih (Piper Betle L.) Sebagai Pengganti ADP (Adenosine Diphosphate) Pada Pemeriksaan Agregasi Trombosit." Lontara 2, no. 1 (2021): 11–17. http://dx.doi.org/10.53861/lontarariset.v2i1.184.

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Adenosine diphosphate (ADP) reagent is often used in the examination of platelet aggregation, yet has limitations in terms of price and availability. Natural source namely betel leaf (Piper betle L.) are believed to be used as a substitute for ADP because betel leaf have the characteristics of styptic (to resist bleeding), vulnerary (to heal skin wounds), and anti-inflammatory (to preserve inflammation) (Moeljanto & Mulyono, 2003). The aim of this study was to determine the potential of betel leaf on the examination of platelet aggregation. The method used in this research included the bet

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Turner, Nancy A., Joel L. Moake, and Larry V. McIntire. "Blockade of adenosine diphosphate receptors P2Y12 and P2Y1 is required to inhibit platelet aggregation in whole blood under flow." Blood 98, no. 12 (2001): 3340–45. http://dx.doi.org/10.1182/blood.v98.12.3340.

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Abstract Using heparinized whole blood and flow conditions, it was shown that adenosine 5′-diphosphate (ADP) receptors P2Y12 and P2Y1 are both important in direct shear-induced platelet aggregation and platelet aggregation subsequent to initial adhesion onto von Willebrand factor (vWf)–collagen. In the viscometer, whole blood was subjected to shear rates of 750, 1500, and 3000 s−1 for 30 seconds at room temperature. The extent of aggregation was determined by flow cytometry. The P2Y12antagonist AR-C69 931MX (ARMX) reduced shear-induced aggregation at these rates by 56%, 54%, and 16%, respectiv

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Leon, Catherine, Meike Alex, Antje Klocke, et al. "Platelet ADP receptors contribute to the initiation of intravascular coagulation." Blood 103, no. 2 (2004): 594–600. http://dx.doi.org/10.1182/blood-2003-05-1385.

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Abstract While the adenosine 5′-diphosphate (ADP) pathway is known to enhance thrombus formation by recruiting platelets and leukocytes to the primary layer of collagen-adhering platelets, its role for the initiation of coagulation has not been revealed. Ex vivo inhibition of the P2Y12 ADP receptor by clopidogrel administration diminished the rapid exposure of tissue factor (TF), the major initiator of coagulation, in conjugates of platelets with leukocytes established by the contact of whole blood with fibrillar collagen. Under in vitro conditions, the P2Y12 and P2Y1 ADP receptors were both f

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Agarwal, Ashok K., Narendra N. Tandon, Nicholas J. Greco, Noel J. Cusack, and G. A. Jamieson. "Evaluation of the Binding to Fixed Platelets of Agonists and Antagonists of ADP-Induced Aggregation." Thrombosis and Haemostasis 62, no. 04 (1989): 1103–6. http://dx.doi.org/10.1055/s-0038-1647126.

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SummarySteady state binding of eleven different ADP analogues to formaldehyde-fixed platelets has been determined in a competitive binding assay using 3H-ADP. The compounds tested were the inactive analogues L-ADP and L-ATP; the agonists 2-chloroadenosine 5’-diphosphate, adenosine 5’-O-(2-thiodiphosphate)and the diastereoisomeric pair Sp-adenosine 5’-(1-thiodiphosphate) (Sp-ADP-α-S) and Rp-adenosine 5’-(1-thiodiphosphate) (Rp-ADP-α-S); and the antagonists adenosine 5’-O-thiomonophosphate, 2-chloroadenosine 5’-O-thiomonophosphate, 2-chloroadenosine 5’-triphoshate, and the diastereoisomeric pair

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Behrend, EN, GF Grauer, DS Greco, BJ Rose, and MA Thrall. "Comparison of the effects of diltiazem and aspirin on platelet aggregation in cats." Journal of the American Animal Hospital Association 32, no. 1 (1996): 11–18. http://dx.doi.org/10.5326/15473317-32-1-11.

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Platelet aggregation in response to collagen (1 or 3 micrograms/ml), arachidonic acid (10(-2) M), and adenosine diphosphate (ADP, 2 microM) was compared in healthy cats treated with diltiazem (approximately 2 mg/kg body weight, q 8 hrs for 10 doses), aspirin (approximately 21 mg/kg body weight [1 baby aspirin], q 72 hrs for three doses), or a combination of diltiazem and aspirin. Baseline values obtained prior to treatment served as controls. Addition of arachidonic acid to blood resulted in an impedance change (i.e., aggregation) with time in samples from the nontreated cats and the cats trea

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Tolhurst, Gwen, Catherine Vial, Catherine Léon, Christian Gachet, Richard J. Evans, and Martyn P. Mahaut-Smith. "Interplay between P2Y1, P2Y12, and P2X1 receptors in the activation of megakaryocyte cation influx currents by ADP: evidence that the primary megakaryocyte represents a fully functional model of platelet P2 receptor signaling." Blood 106, no. 5 (2005): 1644–51. http://dx.doi.org/10.1182/blood-2005-02-0725.

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Abstract The difficulty of conducting electrophysiologic recordings from the platelet has restricted investigations into the role of ion channels in thrombosis and hemostasis. We now demonstrate that the well-established synergy between P2Y1 and P2Y12 receptors during adenosine diphosphate (ADP)–dependent activation of the platelet αIIbβ3 integrin also exists in murine marrow megakaryocytes, further supporting the progenitor cell as a bona fide model of platelet P2 receptor signaling. In patch clamp recordings, ADP (30 μM) stimulated a transient inward current at –70 mV, which was carried by N

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Coleman, Leon G., Renata K. Polanowska-Grabowska, Marek Marcinkiewicz, and Adrian R. L. Gear. "LDL oxidized by hypochlorous acid causes irreversible platelet aggregation when combined with low levels of ADP, thrombin, epinephrine, or macrophage-derived chemokine (CCL22)." Blood 104, no. 2 (2004): 380–89. http://dx.doi.org/10.1182/blood-2003-08-2961.

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Abstract The in vitro oxidation of low-density lipoprotein (LDL) by hypochlorous acid produces a modified form (HOCl-LDL) capable of stimulating platelet function. We now report that HOCl-LDL is highly effective at inducing platelet function, causing stable aggregation and α-granule secretion. Such stimulation depended on the presence of low levels of primary agonists such as adenosine diphosphate (ADP) and thrombin, or others like epinephrine (EPI) and macrophage-derived chemokine (MDC, CCL22). Agonist levels, which by themselves induced little or reversible aggregation, caused strong stable

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Jedlitschky, Gabriele, Konstanze Tirschmann, Lena E. Lubenow, et al. "The nucleotide transporter MRP4 (ABCC4) is highly expressed in human platelets and present in dense granules, indicating a role in mediator storage." Blood 104, no. 12 (2004): 3603–10. http://dx.doi.org/10.1182/blood-2003-12-4330.

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Platelet aggregation is initiated by the release of mediators as adenosine diphosphate (ADP) stored in platelet granules. Possible candidates for transport proteins mediating accumulation of these mediators in granules include multidrug resistance protein 4 (MRP4, ABCC4), a transport pump for cyclic nucleotides and nucleotide analogs. We investigated the expression of MRP4 in human platelets by immunoblotting, detecting a strong signal at 170 kDa. Immunofluorescence microscopy using 2 MRP4-specific antibodies revealed staining mainly in intracellular structures, which largely colocalized with

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Pero, Ronald W., Leif G. Salford, Lars-Göran Strömblad, and Christina Andersson. "Mononuclear leukocyte ADP-ribosylation as an indicator of immune function in malignant-glioma patients treated with betamethasone for cerebral edema." Journal of Neurosurgery 77, no. 4 (1992): 601–6. http://dx.doi.org/10.3171/jns.1992.77.4.0601.

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✓ Glioma patients receiving corticosteroids (16 mg/day betamethasone) were examined for evidence of immune cell dysfunction by using quantitative estimates of adenosine diphosphate (ADP)-ribosylation in peripheral mononuclear leukocytes as the physiological indicator. The duration of daily treatment with corticosteroids varied from 0 to 35 days at the time of collection of the blood samples. Even after adjustment for covariate factors such as age, sex, smoking habits, alcohol use, antiepileptic medications, and tumor grade, there still remained a highly significant dose-dependent inverse relat

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Driessens, MH, EA van Rijthoven, G. La Riviere, and E. Roos. "Expression of pertussis toxin adenosine diphosphate-ribosyltransferase in a T-cell hybridoma reduces metastatic capacity." Blood 88, no. 8 (1996): 3116–23. http://dx.doi.org/10.1182/blood.v88.8.3116.bloodjournal8883116.

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T-cell hybridomas are highly metastatic, and their in vitro invasiveness correlates with metastatic capacity. Invasion is blocked by pertussis toxin (PT), which adenosine diphosphate (ADP)-ribosylates G1-proteins, and we have provided evidence that the PT-sensitive signal stimulates leukocyte function-associated antigen-1 (LFA-1)-mediated adhesion required for invasion. PT pretreatment of TAM2D2 T-cell hybridoma cells reduced metastasis, but only to a limited extent. In the present study, we have transfected the cDNA of the PT ADP-ribosyltransferase S1 subunit into TAM2D2 cells to abrogate G1-

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Brzoska, Tomasz, Egemen Tutuncuoglu, Stevan P. Tofovic, Edwin K. Jackson, Mark T. Gladwin, and Prithu Sundd. "CD39 As a Master Regulator of Pulmonary Thrombosis in Sickle Cell Disease." Blood 134, Supplement_1 (2019): 2266. http://dx.doi.org/10.1182/blood-2019-130882.

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Acute systemic painful vaso-occlusive crisis (VOC) often serves as an antecedent to acute chest syndrome (ACS), which is a type of acute lung injury and the leading cause of mortality among sickle cell disease (SCD) patients. Thrombocytopenia secondary to pulmonary thrombosis is major risk factor for ACS, however, only 20% of ACS patients are diagnosed with pulmonary thrombosis as an underlying cause of ACS. Although clinical evidence supports the presence of prothrombotic state in subset of SCD patients, the molecular, cellular and genetic mechanisms that selectively render subset of SCD pati

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Jones, Chris I., Sarah Bray, Stephen F. Garner, et al. "A functional genomics approach reveals novel quantitative trait loci associated with platelet signaling pathways." Blood 114, no. 7 (2009): 1405–16. http://dx.doi.org/10.1182/blood-2009-02-202614.

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AbstractPlatelet response to activation varies widely between individuals but shows interindividual consistency and strong heritability. The genetic basis of this variation has not been properly explored. We therefore systematically measured the effect on function of sequence variation in 97 candidate genes in the collagen and adenosine-diphosphate (ADP) signaling pathways. Resequencing of the genes in 48 European DNA samples nearly doubled the number of known single nucleotide polymorphisms (SNPs) and informed the selection of 1327 SNPs for genotyping in 500 healthy Northern European subjects

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Gubin, Alexander N., J. Muthoni Njoroge, Urszula Wojda, et al. "Identification of the Dombrock blood group glycoprotein as a polymorphic member of the ADP-ribosyltransferase gene family." Blood 96, no. 7 (2000): 2621–27. http://dx.doi.org/10.1182/blood.v96.7.2621.

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Abstract Identification of the 25 known human blood group molecules is of fundamental importance for the fields of erythroid cell biology and transfusion medicine. Here we provide the first molecular description of the “Dombrock” blood group system. A candidate gene was identified by in silico analyses of approximately 5000 expressed sequence tags (ESTs) from terminally differentiating human erythroid cells. Transfection experiments demonstrated specific binding of anti-Dombrock and confirmed glycosylphosphatidylinositol membrane attachment. Dombrock expression is developmentally regulated dur

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Gubin, Alexander N., J. Muthoni Njoroge, Urszula Wojda, et al. "Identification of the Dombrock blood group glycoprotein as a polymorphic member of the ADP-ribosyltransferase gene family." Blood 96, no. 7 (2000): 2621–27. http://dx.doi.org/10.1182/blood.v96.7.2621.h8002621_2621_2627.

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Identification of the 25 known human blood group molecules is of fundamental importance for the fields of erythroid cell biology and transfusion medicine. Here we provide the first molecular description of the “Dombrock” blood group system. A candidate gene was identified by in silico analyses of approximately 5000 expressed sequence tags (ESTs) from terminally differentiating human erythroid cells. Transfection experiments demonstrated specific binding of anti-Dombrock and confirmed glycosylphosphatidylinositol membrane attachment. Dombrock expression is developmentally regulated during eryth

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Cristalli, G., and D. C. B. Mills. "Identification of a receptor for ADP on blood platelets by photoaffinity labelling." Biochemical Journal 291, no. 3 (1993): 875–81. http://dx.doi.org/10.1042/bj2910875.

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The synthesis of a new analogue of ADP, 2-(p-azidophenyl)-ethythioadenosine 5′-diphosphate (AzPET-ADP), is described. This compound contains a photolabile phenylazide group attached to the ADP molecule by a thioether link at the purine 2 position. It has been prepared in radioactive form with 32P in the beta-phosphate at a specific radioactivity of 100 mCi/mumol. The reagent activated platelets, causing shape change and aggregation, with somewhat lower affinity than ADP. On photolysis the affinity was increased. The reagent also inhibited platelet adenylate cyclase stimulation by prostaglandin

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Podczasy, John J., James Lee, and Ivana Vucenik. "Evaluation of Whole-Blood Lumiaggregation." Clinical and Applied Thrombosis/Hemostasis 3, no. 3 (1997): 190–95. http://dx.doi.org/10.1177/107602969700300307.

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An evaluation of whole-blood lumiaggregation was conducted in a normal population. Platelet aggregation and adenosine triphosphate (ATP) secretion were monitored in a three-phase study that analyzed sample dilution, agonist dose response, and method comparison. In the first phase, the blood:saline ratio was varied; in the second phase, the concentration of the agonists was varied ; and in the last phase, a comparison of impedance aggregation and ATP release in whole blood to optical aggregation and ATP release in platelet-rich plasma (PRP) was performed. Five common platelet agonists— collagen

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Sharp, Dan S., Neal L. Benowitz, P. M. W. Bath, John F. Martin, Andrew D. Beswick, and Peter C. Elwood. "Cigarette Smoking Sensitizes and Desensitizes Impedance-measured ADP-induced Platelet Aggregation in Whole Blood." Thrombosis and Haemostasis 74, no. 02 (1995): 730–35. http://dx.doi.org/10.1055/s-0038-1649805.

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SummaryThe effect of smoking on platelet aggregation appears to produce conflicting results, with some studies indicating an enhancement and others a decrease of aggregation. This epidemiological study of 120 male smokers, a subset of the Caerphilly Heart Disease Study, examined the relationship of two dimensions of smoking (time proximity of last cigarette before venepuncture and serum nicotine concentration) with threshold dose of adenosine diphosphate (ADP) necessary to induce platelet aggregation in whole blood. Means (range) of ADP threshold dose and nicotine concentration were 1.66 (0.5-

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Jones, GD, and AR Gear. "Subsecond calcium dynamics in ADP- and thrombin-stimulated platelets: a continuous-flow approach using indo-1." Blood 71, no. 6 (1988): 1539–43. http://dx.doi.org/10.1182/blood.v71.6.1539.1539.

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Abstract The regulation and kinetics (less than 5 seconds) of cytosolic calcium changes ([Ca2+]i) in stimulated blood platelets have been investigated under physiological blood flow conditions. Using a newly-developed continuous-flow approach with indo-1-loaded human platelets, adenosine diphosphate (ADP, 10 mumol/L) and thrombin (5 U/mL) were equally effective in significantly increasing [Ca2+]i by 0.5 seconds. ADP induced a transient [Ca2+]i peak of 1 to 2 mumol/L near 2 seconds, whereas thrombin caused a sustained and larger response. The first phase (less than 2 seconds) was not influenced

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37

Jones, GD, and AR Gear. "Subsecond calcium dynamics in ADP- and thrombin-stimulated platelets: a continuous-flow approach using indo-1." Blood 71, no. 6 (1988): 1539–43. http://dx.doi.org/10.1182/blood.v71.6.1539.bloodjournal7161539.

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The regulation and kinetics (less than 5 seconds) of cytosolic calcium changes ([Ca2+]i) in stimulated blood platelets have been investigated under physiological blood flow conditions. Using a newly-developed continuous-flow approach with indo-1-loaded human platelets, adenosine diphosphate (ADP, 10 mumol/L) and thrombin (5 U/mL) were equally effective in significantly increasing [Ca2+]i by 0.5 seconds. ADP induced a transient [Ca2+]i peak of 1 to 2 mumol/L near 2 seconds, whereas thrombin caused a sustained and larger response. The first phase (less than 2 seconds) was not influenced by a lac

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38

Alkhamis, TM, RL Beissinger, and JR Chediak. "Artificial surface effect on red blood cells and platelets in laminar shear flow." Blood 75, no. 7 (1990): 1568–75. http://dx.doi.org/10.1182/blood.v75.7.1568.1568.

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Abstract Red blood cell (RBC) effects on platelet adhesion to a nonbiologic test surface (tetrafluoroethylene propylene copolymer) and platelet aggregation during laminar shear flow for shear rates to 5,680 s-1 (corresponding to shear stress to 200 dyne/cm2) were investigated. Results on hemoglobin (Hb) and adenosine diphosphate (ADP) release from RBCs, percent decrease of single platelets in the bulk, and percent of test surface covered with platelets were obtained in a cone-and-plate (CP) viscometer for samples of whole blood, suspensions of RBC ghosts in platelet-rich plasma (PRP), and susp

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39

Alkhamis, TM, RL Beissinger, and JR Chediak. "Artificial surface effect on red blood cells and platelets in laminar shear flow." Blood 75, no. 7 (1990): 1568–75. http://dx.doi.org/10.1182/blood.v75.7.1568.bloodjournal7571568.

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Red blood cell (RBC) effects on platelet adhesion to a nonbiologic test surface (tetrafluoroethylene propylene copolymer) and platelet aggregation during laminar shear flow for shear rates to 5,680 s-1 (corresponding to shear stress to 200 dyne/cm2) were investigated. Results on hemoglobin (Hb) and adenosine diphosphate (ADP) release from RBCs, percent decrease of single platelets in the bulk, and percent of test surface covered with platelets were obtained in a cone-and-plate (CP) viscometer for samples of whole blood, suspensions of RBC ghosts in platelet-rich plasma (PRP), and suspensions o

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40

Battinelli, Elisabeth M., Beth A. Markens, and Joseph E. Italiano. "Release of angiogenesis regulatory proteins from platelet alpha granules: modulation of physiologic and pathologic angiogenesis." Blood 118, no. 5 (2011): 1359–69. http://dx.doi.org/10.1182/blood-2011-02-334524.

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Abstract An association between platelets, angiogenesis, and cancer has long been recognized, but the mechanisms linking them remains unclear. Platelets regulate new blood vessel growth through numerous stimulators and inhibitors of angiogenesis by several pathways, including differential exocytosis of angiogenesis regulators. Herein, we investigated the differential release of angiogenesis stimulators and inhibitors from platelets. Activation of human platelets with adenosine diphosphate (ADP) stimulated the release of VEGF, but not endostatin whereas, thromboxane A2 (TXA2) released endostati

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Purvis, Jeremy E., Manash S. Chatterjee, Lawrence F. Brass, and Scott L. Diamond. "A molecular signaling model of platelet phosphoinositide and calcium regulation during homeostasis and P2Y1 activation." Blood 112, no. 10 (2008): 4069–79. http://dx.doi.org/10.1182/blood-2008-05-157883.

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Abstract To quantify how various molecular mechanisms are integrated to maintain platelet homeostasis and allow responsiveness to adenosine diphosphate (ADP), we developed a computational model of the human platelet. Existing kinetic information for 77 reactions, 132 fixed kinetic rate constants, and 70 species was combined with electrochemical calculations, measurements of platelet ultrastructure, novel experimental results, and published single-cell data. The model accurately predicted: (1) steady-state resting concentrations for intracellular calcium, inositol 1,4,5-trisphosphate, diacylgly

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Patel, Yatin M., Kirti Patel, Salman Rahman та ін. "Evidence for a role for Gαi1 in mediating weak agonist-induced platelet aggregation in human platelets: reduced Gαi1 expression and defective Gi signaling in the platelets of a patient with a chronic bleeding disorder". Blood 101, № 12 (2003): 4828–35. http://dx.doi.org/10.1182/blood-2002-10-3080.

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AbstractWe have examined platelet functional responses and characterized a novel signaling defect in the platelets of a patient suffering from a chronic bleeding disorder. Platelet aggregation responses stimulated by weak agonists such as adenosine diphosphate (ADP) and adrenaline were severely impaired. In comparison, both aggregation and dense granule secretion were normal following activation with high doses of collagen, thrombin, or phorbol-12 myristate-13 acetate (PMA). ADP, thrombin, or thromboxane A2 (TxA2) signaling through their respective Gq-coupled receptors was normal as assessed b

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43

Pospieszna, Barbara, Krzysztof Kusy, Ewa Maria Słomińska, Wioleta Dudzinska, Monika Ciekot-Sołtysiak, and Jacek Zieliński. "The Effect of Training on Erythrocyte Energy Status and Plasma Purine Metabolites in Athletes." Metabolites 10, no. 1 (2019): 5. http://dx.doi.org/10.3390/metabo10010005.

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This study aimed to assess the changes in red blood cell (RBC) energy status and plasma purine metabolites concentration over a one-year training cycle in endurance-trained (EN; n = 11, 20–26 years), and sprint-trained (SP; n = 11, 20–30 years) competitive athletes in comparison to recreationally-trained individuals (RE; n = 11, 20–26 years). Somatic, physiological, and biochemical variables were measured in four training phases differing in exercise load profile: transition, general, specific, and competition. Significantly highest values of RBC adenylate energy charge (AEC; p ≤ 0.001), ATP-t

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Weiss, HJ, B. Lages, T. Hoffmann, and VT Turitto. "Correction of the platelet adhesion defect in delta-storage pool deficiency at elevated hematocrit--possible role of adenosine diphosphate." Blood 87, no. 10 (1996): 4214–22. http://dx.doi.org/10.1182/blood.v87.10.4214.bloodjournal87104214.

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Previous studies on patients with storage pool deficiency (SPD) who are specifically deficient in platelet dense granules (delta-SPD) have suggested a role for dense granule substances, in all likelihood adenosine diphosphate (ADP), in mediating thrombus formation on subendothelium at high shear rates. The role of dense granule substances in mediating platelet adhesion appears to be more complicated Previous studies in delta-SPD suggested an adhesion defect that was strongly influenced by the patient's hematocrit (Hct) value. To explore further the possibility that red blood cells (RBCs) may i

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Bult, Hidde, Hermine R. L. Fret, François H. Jordaens, and Arnold G. Herman. "Dipyridamole Potentiates Platelet Inhibition by Nitric Oxide." Thrombosis and Haemostasis 66, no. 03 (1991): 343–49. http://dx.doi.org/10.1055/s-0038-1646418.

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SummaryIn a placebo-controlled double blind cross-over experiment the adenosine uptake inhibitor dipyridamole (400 mg/day) did not affect ex vivo platelet aggregation induced by collagen or adenosine-diphosphate (ADP) in an electronic whole blood aggregometer (WBA). Dipyridamole was also inactive in vitro, unless red blood cell injury was deliberately enhanced, thereby increasing the level of free adenine nucleotides. Since dipyridamole also inhibits cyclic guanosine monophosphate (GMP) phosphodiesterase (PDE), we used platelet rich plasma (PRP) to study its interaction with authentic and endo

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46

Funaro, Ada, Erika Ortolan, Bruna Ferranti, et al. "CD157 is an important mediator of neutrophil adhesion and migration." Blood 104, no. 13 (2004): 4269–78. http://dx.doi.org/10.1182/blood-2004-06-2129.

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Abstract CD157, a glycosylphosphatidylinositol (GPI)–anchored protein encoded by a member of the CD38 NADase/ADP-ribosyl cyclase gene family, is expressed on the surface of most human circulating neutrophils. This work demonstrates that CD157 is a receptor that induces reorganization of the cytoskeleton and significant changes in cell shape, and that signals mediated by CD157 act through modulation of cytosolic Ca2+ concentration. These signals are independent of the products of CD157's enzymatic activities (ie, cyclic adenosine diphosphate [ADP]–ribose and ADP-ribose). Indeed, the enzymatic a

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47

Pengo, V., M. Boschello, P. Prandoni, L. Schivazappa та A. Girolami. "Beta-thromboglobulin (β-TG) and platelet factor 4 (PF4) release by adenosine diphosphate (ADP) contact with native whole blood". Thrombosis Research 39, № 5 (1985): 645–50. http://dx.doi.org/10.1016/0049-3848(85)90247-6.

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Mazzucato, Mario, Paola Pradella, Maria Rita Cozzi, Luigi De Marco та Zaverio M. Ruggeri. "Sequential cytoplasmic calcium signals in a 2-stage platelet activation process induced by the glycoprotein Ibα mechanoreceptor". Blood 100, № 8 (2002): 2793–800. http://dx.doi.org/10.1182/blood-2002-02-0514.

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We found that the interaction of platelets with immobilized von Willebrand factor (VWF) under flow induces distinct elevations of cytosolic Ca++ concentration ([Ca++]i) that are associated with sequential stages of integrin αIIbβ3 activation. Fluid-dynamic conditions that are compatible with the existence of tensile stress on the bonds between glycoprotein Ibα (GPIbα) and the VWF A1 domain led to Ca++ release from intracellular stores (type α/β peaks), which preceded stationary platelet adhesion. Raised levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate, as well

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Refaai, Majed A., Kelly F. Henrichs, Sherry L. Spinelli, et al. "Platelet Activation Following Exposure to Anti-ABO Antibodies— An In Vitro Study." Oncology & Hematology Review (US) 07, no. 01 (2011): 72. http://dx.doi.org/10.17925/ohr.2011.07.1.72.

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Since platelets possess A and B antigen, mismatched ABO platelets could, theoretically, become activated or hypofunctional by exposure to anti-A or anti-B antibodies found in transfused or recipient plasma. Following normal baseline platelet aggregation to adenosine diphosphate (ADP), platelets from normal donors of different blood types were incubated at 37°C for 10 minutes with 50μl of normal saline (NS), O plasma, or AB plasma. Aggregation was then induced with ADP. No significant changes from baseline were seen in platelet aggregation studies following incubation with NS. However, platelet

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50

Cattaneo, Marco. "Bleeding manifestations of congenital and drug-induced defects of the platelet P2Y12 receptor for adenosine diphosphate." Thrombosis and Haemostasis 105, S 06 (2011): S67—S74. http://dx.doi.org/10.1160/ths10-11-0742.

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SummaryP2Y12, one of the two platelet receptors for adenosine diphosphate (ADP), plays a central role in platelet function. Defects of P2Y12 should be suspected when ADP, even at high concentrations (≥10 μM), is unable to induce full, irreversible platelet aggregation. Patients with congenital P2Y12 defects display a mild-to-moderate bleeding diathesis of variable severity, characterised by mucocutaneous bleeding and excessive post-surgical and post-traumatic blood loss. Drugs that inhibit P2Y12 are potent antithrombotic drugs, attesting the central role played by P2Y12 in platelet thrombus fo

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