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Journal articles on the topic 'PLATELET AGGREGATION INHIBITORS/analysis'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Kazes, Isabelle, Ismaı̈l Elalamy, Jean-Daniel Sraer, Mohamed Hatmi, and Geneviève Nguyen. "Platelet release of trimolecular complex components MT1-MMP/TIMP2/MMP2: involvement in MMP2 activation and platelet aggregation." Blood 96, no. 9 (2000): 3064–69. http://dx.doi.org/10.1182/blood.v96.9.3064.

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Abstract Matrix metalloproteinase 2 (MMP2) has been reported to be secreted by collagen-stimulated platelets, and active MMP2 has been shown to play a role in platelet aggregation. It has been demonstrated that MMP2 activation is dependent on the complex (membrane type 1 [MT1]-MMP/tissue inhibitor of MMP2 [TIMP2]) receptor and MMP2. We have investigated human platelets as a possible source of MT1-MMP, and we have studied its role in MMP2 activation and in platelet aggregation. Gelatin zymograms showed the existence of MMP2 at proforms (68 kd) and activated-enzyme forms (62-59 kd) in supernatan

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2

Kazes, Isabelle, Ismaı̈l Elalamy, Jean-Daniel Sraer, Mohamed Hatmi, and Geneviève Nguyen. "Platelet release of trimolecular complex components MT1-MMP/TIMP2/MMP2: involvement in MMP2 activation and platelet aggregation." Blood 96, no. 9 (2000): 3064–69. http://dx.doi.org/10.1182/blood.v96.9.3064.h8003064_3064_3069.

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Matrix metalloproteinase 2 (MMP2) has been reported to be secreted by collagen-stimulated platelets, and active MMP2 has been shown to play a role in platelet aggregation. It has been demonstrated that MMP2 activation is dependent on the complex (membrane type 1 [MT1]-MMP/tissue inhibitor of MMP2 [TIMP2]) receptor and MMP2. We have investigated human platelets as a possible source of MT1-MMP, and we have studied its role in MMP2 activation and in platelet aggregation. Gelatin zymograms showed the existence of MMP2 at proforms (68 kd) and activated-enzyme forms (62-59 kd) in supernatants of res

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3

Jurasz, Paul, David Alonso, Susana Castro-Blanco, Ferid Murad, and Marek W. Radomski. "Generation and role of angiostatin in human platelets." Blood 102, no. 9 (2003): 3217–23. http://dx.doi.org/10.1182/blood-2003-02-0378.

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AbstractPlatelets regulate new blood vessel growth, because they contain a number of angiogenesis promoters and inhibitors. Additionally, platelets contain matrix metalloproteinases (MMPs), which when released mediate platelet adhesion and aggregation, and plasminogen, a fibrinolytic system enzyme that serves to limit blood clot formation. Enzymatic cleavage of plasminogen by MMPs generates angiostatin, an angiogenesis inhibitor. Therefore, we examined whether platelets generate angiostatin during aggregation in vitro. Platelets were isolated from healthy human donors and then aggregated with

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4

Fijnheer, Rob, Martine N. Boomgaard, Alfons J. M. van den Eertwegh, et al. "Stored Platelets Release Nucleotides as Inhibitors of Platelet Function." Thrombosis and Haemostasis 68, no. 05 (1992): 595–99. http://dx.doi.org/10.1055/s-0038-1646323.

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SummaryIt is well known that the function of platelets decreases progressively during storage of platelet concentrates at room temperature. To investigate this phenomenon in more detail, we have resuspended platelets that had been stored for 24 h or 72 h in fresh plasma, and we have measured the aggregation response and the ATP secretion. Conversely, the effect of plasma in which platelet concentrates (PC) had been stored for 24 h or 72 h, was tested on fresh platelets. Both the aggregation response to collagen and ADP and the collagen-induced ATP secretion of stored platelets partially recove

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5

Alevriadou, BR, JL Moake, NA Turner, et al. "Real-time analysis of shear-dependent thrombus formation and its blockade by inhibitors of von Willebrand factor binding to platelets." Blood 81, no. 5 (1993): 1263–76. http://dx.doi.org/10.1182/blood.v81.5.1263.1263.

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Abstract Two likely mechanisms for the initiation of arterial platelet thrombus formation under conditions of elevated fluid shear stresses are: (1) excessive adhesion and aggregation of platelets from rapidly flowing blood onto the exposed sub-endothelium of injured, atherosclerotic arteries; or (2) direct, fluid shear stress-induced aggregation of platelets in constricted arteries with intact endothelial cells. Mechanism (1) was simulated using a parallel plate flow chamber, fibrillar collagen type I-coated slides, and mepacrine-labeled (fluorescent) platelets in whole blood anticoagulated w

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Alevriadou, BR, JL Moake, NA Turner, et al. "Real-time analysis of shear-dependent thrombus formation and its blockade by inhibitors of von Willebrand factor binding to platelets." Blood 81, no. 5 (1993): 1263–76. http://dx.doi.org/10.1182/blood.v81.5.1263.bloodjournal8151263.

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Two likely mechanisms for the initiation of arterial platelet thrombus formation under conditions of elevated fluid shear stresses are: (1) excessive adhesion and aggregation of platelets from rapidly flowing blood onto the exposed sub-endothelium of injured, atherosclerotic arteries; or (2) direct, fluid shear stress-induced aggregation of platelets in constricted arteries with intact endothelial cells. Mechanism (1) was simulated using a parallel plate flow chamber, fibrillar collagen type I-coated slides, and mepacrine-labeled (fluorescent) platelets in whole blood anticoagulated with citra

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7

Shankar, Haripriya, Swaminathan Murugappan, Soochong Kim, et al. "Role of G protein–gated inwardly rectifying potassium channels in P2Y12 receptor–mediated platelet functional responses." Blood 104, no. 5 (2004): 1335–43. http://dx.doi.org/10.1182/blood-2004-01-0069.

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Abstract The role of the Gi-coupled platelet P2Y12 receptor in platelet function has been well established. However, the functional effector or effectors contributing directly to αIIbβ3 activation in human platelets has not been delineated. As the P2Y12 receptor has been shown to activate G protein–gated, inwardly rectifying potassium (GIRK) channels, we investigated whether GIRK channels mediate any of the functional responses of the platelet P2Y12 receptor. Western blot analysis revealed that platelets express GIRK1, GIRK2, and GIRK4. In aspirin-treated and washed human platelets, 2 structur

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8

Aslan, Joseph E., Kevin G. Phillips, Laura D. Healy, Asako Itakura, Jiaqing Pang та Owen J. T. McCarty. "Histone deacetylase 6-mediated deacetylation of α-tubulin coordinates cytoskeletal and signaling events during platelet activation". American Journal of Physiology-Cell Physiology 305, № 12 (2013): C1230—C1239. http://dx.doi.org/10.1152/ajpcell.00053.2013.

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The tubulin cytoskeleton plays a key role in maintaining the characteristic quiescent discoid shape of resting platelets. Upon activation, platelets undergo a dramatic change in shape; however, little is known of how the microtubule system contributes to regulating platelet shape and function. Here we investigated the role of the covalent modification of α-tubulin by acetylation in the regulation of platelet physiology during activation. Superresolution microscopy analysis of the platelet tubulin cytoskeleton showed that the marginal band together with an interconnected web of finer tubulin st

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9

Jackson, Shaun P. "The growing complexity of platelet aggregation." Blood 109, no. 12 (2007): 5087–95. http://dx.doi.org/10.1182/blood-2006-12-027698.

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Abstract Platelet aggregation, the process by which platelets adhere to each other at sites of vascular injury, has long been recognized as critical for hemostatic plug formation and thrombosis. Until relatively recently, platelet aggregation was considered a straightforward process involving the noncovalent bridging of integrin αIIbβ3 receptors on the platelet surface by the dimeric adhesive protein fibrinogen. However, with recent technical advances enabling real-time analysis of platelet aggregation in vivo, it has become apparent that this process is much more complex and dynamic than prev

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10

Dickerson, Matthew, Amber Lee, Anne Hale, and Keith A. Moskowitz. "Lyophilized Human Platelets Restore Hemostasis in the Presence of the P2Y12 Inhibitors Cangrelor, Ticagrelor and Clopidogrel." Blood 136, Supplement 1 (2020): 25. http://dx.doi.org/10.1182/blood-2020-141950.

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• Background: P2Y12 inhibitors block platelet ADP receptors thereby reducing clotting capacity. In an emergency, these agents must be reversed or therapeutically overcome to stop bleeding. Additionally, prior to and during elective procedures these inhibitors must be withdrawn, thereby increasing thrombotic risk. Lyophilized human platelets (Thrombosomes®) are stabilized platelet derived hemostatic agents currently under Phase 2 clinical development for thrombocytopenia and have potential as antiplatelet reversal agents. • Aims: The aim of this study was to determine if lyophilized human plate

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11

Minamoto, Yoko, Takaaki Hato, Shingo Nakatani, and Shigeru Fujita. "Detection of Platelet Adhesion/Aggregation to Immobilized Ligands on Microbeads by an Aggregometer." Thrombosis and Haemostasis 76, no. 06 (1996): 1072–79. http://dx.doi.org/10.1055/s-0038-1650708.

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SummaryPlatelet aggregation is believed to follow platelet adhesion to vascular injury sites. We have developed a turbidimetric assay for platelet aggregation following platelet adhesion to immobilized ligands using an aggregometer. The addition of polystyrene beads coated with von Willebrand factor (vWF) or fibrinogen (Fg) to platelet suspensions caused prompt aggregation of beads and platelets, which was detected as an increase in light transmission. Electron microscopic analysis revealed that platelets adhered to the bead surfaces and that additional platelets adhered to already adhering pl

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12

Moroi, M., SM Jung, K. Shinmyozu, Y. Tomiyama, A. Ordinas, and M. Diaz-Ricart. "Analysis of platelet adhesion to a collagen-coated surface under flow conditions: the involvement of glycoprotein VI in the platelet adhesion." Blood 88, no. 6 (1996): 2081–92. http://dx.doi.org/10.1182/blood.v88.6.2081.bloodjournal8862081.

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Platelet adhesion to the exposed surface of the extracellular matrix in flowing blood is the first and critical reaction for in vivo thrombus formation. However, the mechanism of this in vivo platelet adhesion has yet to be studied extensively. One of the reasons for this is the lack of a practical assay method for assessing platelet adhesion under flow conditions. We have devised an assay method (the fluorescent adhesion assay) that is based on the technique originally reported by Hubbell and McIntire (Biomaterials 7:354, 1986) with some modifications to make it more amenable for assaying sma

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13

Kaiser, William J., Tanya Sage, Parvathy Sasikumar, et al. "Heat Shock Protein 47: A New Platelet Collagen Receptor." Blood 116, no. 21 (2010): 158. http://dx.doi.org/10.1182/blood.v116.21.158.158.

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Abstract Abstract 158 We recently reported that Heat shock protein 47 (Hsp47), a well established collagen binding protein, was present on the surface of human platelets. In the current study we demonstrate that anti-Hsp47 antibodies and a small molecule inhibitor of Hsp47 selectively prevent aggregation of platelets induced with collagen fibrils. Inhibition of Hsp47 was also found to reduce the size of thrombi produced upon perfusion of blood under arterial flow conditions over collagen in vitro. Inclusion of Integrilin, to prevent platelet-platelet interactions via fibrinogen, indicated that

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14

Alderman, Christopher P., Prabha Seshadri, and David I. Ben-Tovim. "Effects of Serotonin Reuptake Inhibitors on Hemostasis." Annals of Pharmacotherapy 30, no. 11 (1996): 1232–34. http://dx.doi.org/10.1177/106002809603001103.

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OBJECTIVE: To examine the hematologic safety profile of the selective serotonin reuptake inhibitors (SSRIs), with particular emphasis on the effects of these drugs on platelet aggregation. METHODS: Platelet aggregation studies were undertaken at baseline, and repeated 2 and 4 weeks after the initiation of treatment with an SSRI. Other investigations undertaken included analysis of serum electrolyte and liver enzyme concentrations, complete blood count, and coagulation studies. Patients were also assessed for clinical signs of bleeding. Eight patients (7 treated with fluoxetine, 1 with paroxeti

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15

Ivandic, B., and N. Frey. "Neue Ansätze und Indikationen zur Plättchenfunktionsdiagnostik in der Kardiologie." Hämostaseologie 31, no. 02 (2011): 73–76. http://dx.doi.org/10.5482/ha-1141.

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SummaryInhibiting platelet function is a key therapeutic principle in cardiology because platelets play a pivotal role in triggering cardiovascular events. In addition to acetylsalicylic acid, a cyclooxygenase inhibitor, ADP-receptor blockers are frequently used for anti-platelet therapy. This therapy does not abolish platelet activation and aggregation. Platelets may still be activated by alternative routes such as the thrombin receptor-mediated pathway. New, more potent inhibitors of platelet function continue to lower the risk of ischaemic events but several trials and clinical registries h

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16

Shiraga, Masamichi, Yoshiaki Tomiyama, Shigenori Honda та ін. "Involvement of Na+/Ca2+ Exchanger in Inside-Out Signaling Through the Platelet Integrin IIbβ3". Blood 92, № 10 (1998): 3710–20. http://dx.doi.org/10.1182/blood.v92.10.3710.

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Abstract The platelet integrin IIbβ3 has become a new target for the treatment of pathological thrombosis. It becomes apparent that the affinity of IIbβ3 for its ligands is dynamically regulated by inside-out signaling. However, the components that couple diverse intracellular signals to the cytoplasmic domains of IIbβ3 remain obscure. Employing a chymotrypsin-induced IIbβ3 activation model, we previously proposed the hypothesis that Na+/Ca2 +exchanger (NCX) may be involved in inside-out signaling (Shiraga et al:Blood 88:2594, 1996). In the present study, employing two unrelated Na+/Ca2+ e

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17

Shiraga, Masamichi, Yoshiaki Tomiyama, Shigenori Honda та ін. "Involvement of Na+/Ca2+ Exchanger in Inside-Out Signaling Through the Platelet Integrin IIbβ3". Blood 92, № 10 (1998): 3710–20. http://dx.doi.org/10.1182/blood.v92.10.3710.422k13_3710_3720.

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The platelet integrin IIbβ3 has become a new target for the treatment of pathological thrombosis. It becomes apparent that the affinity of IIbβ3 for its ligands is dynamically regulated by inside-out signaling. However, the components that couple diverse intracellular signals to the cytoplasmic domains of IIbβ3 remain obscure. Employing a chymotrypsin-induced IIbβ3 activation model, we previously proposed the hypothesis that Na+/Ca2 +exchanger (NCX) may be involved in inside-out signaling (Shiraga et al:Blood 88:2594, 1996). In the present study, employing two unrelated Na+/Ca2+ exchange i

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18

Li, Zhenyu, Guoying Zhang, Hong Yin, Robert Feil, Franz Hofmann, and Xiaoping Du. "The Role of the cGMP-Dependent Protein Kinase II in Platelet Activation and In Vivo Thrombosis." Blood 106, no. 11 (2005): 653. http://dx.doi.org/10.1182/blood.v106.11.653.653.

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Abstract Although it was previously believed that the intracellular secondary messenger cGMP inhibits platelets, we have recently shown that cGMP-dependent protein kinase I (PKG I) in fact plays a stimulatory role in platelet activation. However, there are apparent differences between the PKG inhibitors and PKG I knockout in their effects on platelet activation. PKG inhibitors are more potent in inhibiting platelet activation than PKG I knockout. More importantly, although platelet secretion and aggregation induced by collagen were inhibited by PKG inhibitors, they are not significantly affect

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19

Ortega, Arantxa, Ma Teresa Pérez de Prada, Petra J. Mateos-Cáceres, et al. "Effect of parathyroid-hormone-related protein on human platelet activation." Clinical Science 113, no. 7 (2007): 319–27. http://dx.doi.org/10.1042/cs20070010.

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Evidence suggests that PTHrP [PTH (parathyroid hormone)-related protein] can act as an inflammatory mediator in several pathological settings including cardiovascular disease. The aim of the present study was to determine whether PTHrP might be involved in human platelet activation. We used a turbidimetric method to determine platelet aggregation. The expression of PTH1R (PTH type 1 receptor) in human platelets was analysed by Western blot and flow cytometry analyses. PTHrP-(1–36) (10−7 mol/l) by itself failed to modify the activation of platelets. However, it significantly enhanced ADP-induce

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Quintas-Cardama, Alfonso, Xin Han, Hagop Kantarjian, and Jorge Cortes. "Dasatinib-Induced Platelet Dysfunction." Blood 110, no. 11 (2007): 2941. http://dx.doi.org/10.1182/blood.v110.11.2941.2941.

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Abstract Dasatinib is efficacious and safe in patients (pts) with chronic myelogenous leukemia (CML) after imatinib failure. However, dasatinib therapy has been linked to bleeding in some pts, typically affecting mucosal surfaces. We analyzed the effect of dasatinib on basic coagulation tests and platelet aggregation function in 55 pts with CML in chronic phase at diagnosis (1), >8 weeks after tyrosine kinase inhibitor (TKI) discontinuation (3), or during therapy with the ABL/SRC inhibitors dasatinib (n=27) and bosutinib (n=12), or the aminopyrimidine derivatives imatinib (n=8) and nilotini

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21

Ma, Liping, Xiaoyan Liu, Hongyun Liu, et al. "TLR2-PI3K/Akt Signaling Pathway Involved in Platelet Activation Induced By Group B Streptococci." Blood 126, no. 23 (2015): 4635. http://dx.doi.org/10.1182/blood.v126.23.4635.4635.

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Abstract Background Platelets not only play an important role in the initiation of hemostasis and thrombosis, but also participate in the immune and inflammatory response. Most studies focus on the platelets-bacteria interaction and demonstrate that bacteria are capable of binding to, aggregating and activating platelets. Human platelets are reported to express several groups of TLRs, which participate in the inflammation process and monitoring host infection. Recent data from our laboratory demonstrated that Group B streptococci (GBS) could induce platelet aggregation and up-regulate the expr

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Mason, Christopher, Stephen Lynch, James Benjamin, et al. "Intracellular matrix metalloproteinase-2 (MMP-2) regulates human platelet activation via hydrolysis of talin." Thrombosis and Haemostasis 111, no. 01 (2014): 140–53. http://dx.doi.org/10.1160/th13-03-0248.

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SummaryMatrix metalloproteinase (MMP) activity is generally associated with normal or pathological extracellular processes such as tissue remodeling in growth and development or in tumor metastasis and angiogenesis. Platelets contain at least three MMPs, 1, 2 and 9 that have been reported to stimulate or inhibit agonist-induced platelet aggregation via extracellular signals. The non-selective Zn+2 chelating MMP inhibitor, 1,10-phenanthroline, and the serine protease inhibitor, AEBSF, were found to inhibit all tested agonist-induced platelet aggregation reactions. In vitro analysis demonstrated

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Flaumenhaft, Robert, Lynn VerPlank, James R. Dilks, et al. "Identification of a Novel Par1 inhibitor Using a Chemical Genetic Screen." Blood 116, no. 21 (2010): 2018. http://dx.doi.org/10.1182/blood.v116.21.2018.2018.

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Abstract Abstract 2018 The anucleate platelet is not amenable to traditional forward genetic analysis, but is a good candidate for a chemical genetic screen. In collaboration with the Broad Institute Probe Development Center, we have performed a high throughput screen using a modified luciferin-luciferase detection system to identify inhibitors of Par1-mediated dense granule secretion. For primary screening, over 300,000 compounds were assayed in duplicate using freshly outdated platelet-rich plasma supplied by several blood banks across the United States. Computational analyses of the primary

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Fuentes, Eduardo, Jaime Pereira, Marcelo Alarcón, et al. "Protective Mechanisms ofS. lycopersicumAqueous Fraction (Nucleosides and Flavonoids) on Platelet Activation and Thrombus Formation:In Vitro,Ex VivoandIn VivoStudies." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/609714.

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The purpose of this research was to investigate mechanisms of antiplatelet action of bioactive principle fromS. lycopersicum. Aqueous fraction had a high content of nucleosides (adenosine, guanosine, and adenosine 5′-monophosphate) by HPLC analysis. Also aqueous fraction presented flavonoids content. Aqueous fraction inhibited platelet activation by 15 ± 6% (P<0.05). Fully spread of human platelets on collagen in the presence of aqueous fraction was inhibited from 15 ± 1 to 9 ± 1 μm2(P<0.001). After incubation of whole blood with aqueous fraction, the platelet coverage was inhibited by 5

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Baaten, Constance C. F. M. J., Marieke Sternkopf, Tobias Henning, Nikolaus Marx, Joachim Jankowski, and Heidi Noels. "Platelet Function in CKD: A Systematic Review and Meta-Analysis." Journal of the American Society of Nephrology 32, no. 7 (2021): 1583–98. http://dx.doi.org/10.1681/asn.2020101440.

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BackgroundPatients with CKD are at high risk for thrombotic and hemorrhagic complications. Abnormalities in platelet function are central to these complications, but reports on platelet function in relation to CKD are conflicting, and vary from decreased platelet reactivity to normal or increased platelet responsiveness. The direct effects of uremic toxins on platelet function have been described, with variable findings.MethodsTo help clarify how CKD affects platelet function, we conducted a systematic review and meta-analysis of platelet activity in CKD, with a focus on nondialysis-induced ef

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Brohard-Bohn, Brigitte, Sabine Pain, Christilla Bachelot-Loza, Jacques Auger, and Francine Rendu. "Thiosulfinates Inhibit Platelet Aggregation and Microparticle Shedding at a Calpain-dependent Step." Thrombosis and Haemostasis 86, no. 11 (2001): 1284–91. http://dx.doi.org/10.1055/s-0037-1616063.

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SummaryThiosulfinates (TSs) are sulfur compounds generated through the processing of different Allium species with antiplatelet property. To further define this platelet inhibitory effect we studied diallyl-TS (Al2TS), dipropyl-TS (Pr2TS), and dimethyl-TS (Me2TS) on platelet responses. The three TSs inhibited dose-dependent platelet aggregation, with IC50 values of 15 ± 2, 19 ± 2, and 9 ± 1 μM for Al2TS, Pr2TS and Me2TS, respectively. TSs had no effect on the expression of a platelet procoagulant surface, measured by flow cytometry as the binding of annexin V-FITC. They inhibited the micropart

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van den Kerkhof, Danique L., Paola E. J. van der Meijden, Tilman M. Hackeng та Ingrid Dijkgraaf. "Exogenous Integrin αIIbβ3 Inhibitors Revisited: Past, Present and Future Applications". International Journal of Molecular Sciences 22, № 7 (2021): 3366. http://dx.doi.org/10.3390/ijms22073366.

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The integrin αIIbβ3 is the most abundant integrin on platelets. Upon platelet activation, the integrin changes its conformation (inside-out signalling) and outside-in signalling takes place leading to platelet spreading, platelet aggregation and thrombus formation. Bloodsucking parasites such as mosquitoes, leeches and ticks express anticoagulant and antiplatelet proteins, which represent major sources of lead compounds for the development of useful therapeutic agents for the treatment of haemostatic disorders or cardiovascular diseases. In addition to hematophagous parasites, snakes also poss

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Spertini, Olivier, Jacques Hauert, and Fedor Bachmann. "Reaction of Acetaldehyde with Human Platelets." Thrombosis and Haemostasis 67, no. 01 (1992): 126–30. http://dx.doi.org/10.1055/s-0038-1648393.

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SummaryPlatelet function defects observed in chronic alcoholics are not wholly explained by the inhibitory action of ethanol on platelet aggregation; they are not completely reproduced either in vivo by short-term ethanol perfusion into volunteers or in vitro by the addition of ethanol to platelet-rich plasma. As acetaldehyde (AcH) binds to many proteins and impairs cellular activities, we investigated the effect of this early degradation product of ethanol on platelets. AcH formed adducts with human platelets at neutral pH at 37° C which were stable to extensive washing, trichloracetic acid h

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Lim, Eric, Martin Goddard, Sarah Bellm, et al. "Biological efficacy of low against medium dose aspirin regimen after coronary surgery: Analysis of platelet function." Thrombosis and Haemostasis 95, no. 03 (2006): 476–82. http://dx.doi.org/10.1160/th05-10-0649.

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SummaryThe failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of “aspirin-resistance” remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days.Platelet function was tested the day before surgery and on day+1 and day+5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine.

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Ma, Liping, Qiuhong Yang, Jianxing Chang, Yiqing Li, Liping Zhang, and Xianming Luo. "Inhibition of TLR-4 Prevents From Sepsis-Related eNOS/NO Disturbance in Human Platelets." Blood 118, no. 21 (2011): 5264. http://dx.doi.org/10.1182/blood.v118.21.5264.5264.

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Abstract Abstract 5264 Objective Toll-like receptor 4 (TLR-4) has the ability to activate platelet and involve in intravascular coagulation, inflammatory cytokine and oxidative stressors release in sepsis. Nitric oxide (NO) synthesis in platelets is adjusted by iNOS and/or eNOS and contributes to platelet aggregation and adhesion. Our previous study has found that increased platelet aggregation in patients with sepsis was associated with the expression of TLR4 on platelets and NO synthesis in platelets. This study was to investigate whether inhibition of TLR-4 activation on platelets decreases

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Branchford, Brian R., Susan Sather, Gary Brodsky та ін. "Imer Blocks Phosphorylation of the β3 Integrin, Decreasing Platelet Activation Responses and Protecting Mice From Arterial Thrombosis". Blood 118, № 21 (2011): 189. http://dx.doi.org/10.1182/blood.v118.21.189.189.

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Abstract Abstract 189 Background: Growth Arrest Specific gene 6 (Gas6) signaling through platelet-surface Tyro3/Axl/Mer (TAM) receptors leads to platelet activation and thrombus stabilization. This occurs via activation of phosphatidylinositol-3-kinase (PI3K) and Akt, stimulating tyrosine phosphorylation of the β3 integrin. This process amplifies outside-in signaling via αIIbβ3, which is necessary for stable aggregate formation. iMer is a truncated form of the extracellular domain of the Mer receptor tyrosine kinase, produced by alternative splicing, that inhibits Gas6/TAM signaling, likely by

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Miyake, Tetsuya, Shosaku Nomura, Yutaka Komiyama, et al. "Effect of a New Monoclonal Anti-Glycoprotein IX Antibody, KMP-9, on High Shear-Induced Platelet Aggregation." Thrombosis and Haemostasis 78, no. 02 (1997): 902–9. http://dx.doi.org/10.1055/s-0038-1657650.

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SummaryHuman platelet glycoprotein Ib/IX complex acts as a receptor for von Willebrand factor. It is widely accepted that glycoprotein lb is the essential receptor component, but the role of glycoprotein IX is still unclear. We produced a new monoclonal anti-glycoprotein IX antibody (KMP-9) by the hybridoma technique using platelets from a patient with Glanzmann’s thrombasthenia. The epitope of KMP-9 was localized to the C-terminal 8 kD fragment of glycoprotein IX using ELISA analysis of polyethylene-pin-synthesized peptides, as well as Western blot analysis of platelets after digestion with N

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Dai, Baiyun, Peng Wu, Feng Xue та ін. "Integrin αIIbβ3-Mediated Outside-in Signaling: Brake or Amplifier of Platelet Activation?" Blood 124, № 21 (2014): 4161. http://dx.doi.org/10.1182/blood.v124.21.4161.4161.

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Abstract αIIbβ3 is the most prominent integrin in platelets, and binding to its ligands, in addition to supporting platelet aggregation, also results in the transmission of so-called αIIbβ3-mediated outside-in signals into the cell interior. While it is well accepted that integrin-mediated outside-in signaling functions as an amplifier of platelet activation, accumulating evidence suggests that outside-in signaling can, under certain conditions, function as an inhibitor of platelet activation. In this regard, previous studies have shown that ligand binding and platelet aggregation activate the

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Gao, Cunji, and Peter J. Newman. "PECAM-1 Inhibits Signaling Pathways That Amplify Platelet Aggregation." Blood 108, no. 11 (2006): 1505. http://dx.doi.org/10.1182/blood.v108.11.1505.1505.

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Though protein-tyrosine kinases get most of the attention, there is growing evidence that serine/threonine kinases (S/TKs) also play an important role in amplifying platelet activation responses following exposure to low-dose platelet agonists. For example, granule secretion is markedly impaired in platelets from mice deficient in either isoform of the STKs Akt1 (Blood104:1703, 2004) or Akt2 (J Clin Invest113:441, 2004), and pharmacological inhibition of the mitogen-activated protein kinase, p38, results in greatly reduced platelet aggregation and secretion (JBC271:6586, 1996; Blood107:965, 20

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Aung, Tin Thu Thu, Meng-Yuan Xia, Pyae Phyo Hein, et al. "Chemical Constituents from the Whole Plant of Cuscuta reflexa." Natural Products and Bioprospecting 10, no. 5 (2020): 337–44. http://dx.doi.org/10.1007/s13659-020-00265-x.

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Abstract Two new 2H-pyran-2-one glucosides, cuscutarosides A (1) and B (2), and one new steroidal glucoside, 7β-methoxy-β-sitosterol 3-O-β-glucopyranoside (3), together with 12 known compounds (4–15) were isolated from the whole plant of Cuscuta reflexa (Convolvulaceae) collected from Myanmar. The chemical structures of these new compounds were elucidated based on extensive spectroscopic analysis. The antiobesity activity of these isolates was evaluated using porcine pancreatic lipase (PPL), and the antiplatelet aggregation activity was screened using rabbit platelets induced by thrombin, plat

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Stephens, Gillian, Yibing Yan, Martine Jandrot-Perrus, Jean-Luc Villeval, Kenneth J. Clemetson, and David R. Phillips. "Platelet activation induces metalloproteinase-dependent GP VI cleavage to down-regulate platelet reactivity to collagen." Blood 105, no. 1 (2005): 186–91. http://dx.doi.org/10.1182/blood-2004-07-2842.

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Abstract Glycoprotein (GP) VI, the primary collagen receptor on platelets, has been shown to have variable expression, possibly as a consequence of immune modulation. The present study was designed to determine the mechanism by which GP VI clearance occurs. We found that direct activation of GP VI both by a GP VI–specific antibody and by GP VI ligands (collagen and convulxin) reduced binding of biotinylated convulxin to the stimulated platelets. Analysis of immunoblots of platelets and supernatants showed that the stimulated platelets contained less GP VI, while the soluble fraction contained

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Korte, Wolfgang C., and Giuseppe Plebani. "No Effect of Etodolac, a COX Inhibitor, on Platelet Function in Healthy Volunteers." Blood 110, no. 11 (2007): 2098. http://dx.doi.org/10.1182/blood.v110.11.2098.2098.

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Abstract Background: Avoidance of major bleeding is important with spinal or peridural anaesthesia. Therefore, NSAIDs have to be used with caution in this setting since it has been assumed that with their inhibition of both cyclooxygenase- 1 (COX-1) and cyclooxygenase-2 (COX-2), they increase the risk of reduced platelet aggregagibility and thus bleeding. In contrast, selective COX-2 inhibitiors have no effect on platelet aggregation and can thus be applied up to the point of surgery. The recent withdrawal of Rofecoxib has relaunched the debate on safety of selective COX-2 inhibitors. Etodolac

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Sheu, Joen R., George Hsiao, Hsiung N. Luk, et al. "Mechanisms Involved in the Antiplatelet Activity of Midazolam in Human Platelets." Anesthesiology 96, no. 3 (2002): 651–58. http://dx.doi.org/10.1097/00000542-200203000-00022.

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Background Midazolam is widely used as a sedative and anesthetic induction agent. The aim of this study was to systematically examine the inhibitory mechanisms of midazolam in platelet aggregation. Methods The inhibitory mechanisms of midazolam in platelet aggregation were explored by means of analysis of the platelet glycoprotein IIb-IIIa complex, phosphoinositide breakdown, intracellular Ca+2 mobilization, measurement of membrane fluidity, thromboxane B2 formation, and protein kinase C activity. Results In this study, midazolam dose-dependently (6-26 microm) inhibited platelet aggregation in

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Najeh Al-Saad, Hiba, Ammar Abdul Razzak Mahmood, and Redha I. Al-Bayati. "Design, Synthesis, Docking Study and Antiplatelet Evaluation of New Thiosemicarbazide Derivatives Derived from Captopril." Oriental Journal of Chemistry 35, no. 2 (2019): 829–38. http://dx.doi.org/10.13005/ojc/350246.

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A series of thiosemicarbazide derivatives of captopril, a well-known angiotensin-converting enzyme inhibitor ACEI, have been synthesized by reaction of hydrazide of captopril with different phenylisothiocyanate substituents. The synthesized compounds were characterized using FTIR, 1HNMR and CHNS analysis. The final derivatives were tested for antiplatelet activity using multiplate analyzer and adenosine diphosphate (ADP), arachidonic acid (AA), and collagen, as platelet aggregation inducers. Among tested compounds, derivative 7 and 10 were the most potent inhibitors of platelet aggregation ind

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Panova-Noeva, Marina, Marina Marchetti, Annamaria Leuzzi, et al. "ADP-Induced Whole Blood Aggregometry and Platelet-Associated Thrombin Generation (TG) In Essential Thrombocythemia (ET) and Polycythemia Vera (PV) Patients." Blood 116, no. 21 (2010): 1981. http://dx.doi.org/10.1182/blood.v116.21.1981.1981.

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Abstract Abstract 1981 Patients with ET and PV are characterized by an increased rate of thrombotic complications and by several abnormalities of platelets, more pronounced in JAK2V617F mutation carriers. Platelet function inhibitors are widely utilized for thromboprophylaxis in ET and PV patients. An increased reactivity to ADP of platelets from these patients has previously been shown by light transmission platelet aggregometry studies, which might explain the failure of aspirin to fully protect from thrombosis these patients, mainly those at high risk. While ADP activation pathway is critic

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He, Cui, Lihua Yu, Wenran Dan, et al. "Application of a Simple Microfluidic Chip Analysis Technology to Evaluate the Inhibitory Role of Protocatechuic Acid on Shear-Induced Platelet Aggregation." Evidence-Based Complementary and Alternative Medicine 2021 (May 18, 2021): 1–11. http://dx.doi.org/10.1155/2021/5574413.

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This study aimed to develop a simple microfluidic chip analysis technology to study the inhibitory effect of protocatechuic acid on shear-induced platelet aggregation. The microfluidic chip designed in this study simulates 80% fixed narrow microchannels. This microchannel narrow model uses the finite element analysis module of the three-dimensional modeling software solidwork to analyze fluid dynamic behavior. Blood treated with protocatechuic acid at 1, 2, 4, 8, or 16 µg/mL was passed through the microchannel stenosis model at a shear rate of 10,000 s−1. The platelet adhesion and aggregation

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Siddiqua, Ashia, Michael Wilkinson, Vijay Kakkar, Yatin Patel, Salman Rahman та Kalwant Authi. "Functional Characterization of PM6/13, a β3-specific (GPIIIa/CD61) Monoclonal Antibody that Shows Preferential Inhibition of Fibrinogen Binding over Fibronectin Binding to Activated Human Platelets". Thrombosis and Haemostasis 79, № 01 (1998): 177–85. http://dx.doi.org/10.1055/s-0037-1614247.

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SummaryWe report the characterization of a monoclonal antibody (MAb) PM6/13 which recognises glycoprotein IIIa (GPIIIa) on platelet membranes and in functional studies inhibits platelet aggregation induced by all agonists examined. In platelet-rich plasma, inhibition of aggregation induced by ADP or low concentrations of collagen was accompanied by inhibition of 5-hydroxytryptamine secretion. EC50 values were 10 and 9 [H9262]g/ml antibody against ADP and collagen induced responses respectively. In washed platelets treated with the cyclooxygenase inhibitor, indomethacin, PM6/13 inhibited platel

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Canobbio, Ilaria, Lucia Stefanini, Lina Cipolla та ін. "Genetic Evidence for a Predominant Role of PI3Kβ In ITAM— and Integrin-Mediated Signaling in Platelets". Blood 112, № 11 (2008): 410. http://dx.doi.org/10.1182/blood.v112.11.410.410.

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Abstract Phosphoinositide 3-kinases (PI3K) have been implicated in platelet activation downstream of G protein-coupled receptors (GPCRs), ITAM-bearing receptors, as well as integrins. Among the multiple PI3K isoforms expressed in platelets, PI3Kγ and PI3Kβ are considered to be involved in GPCRs-mediated signaling leading to Rap1b activation and cell aggregation. However, a definitive genetic analysis of the relative contribution of PI3Kβ versus PI3Kγ in the different contexts of platelet activation has not been provided yet. PI3Kγ knockout mice have been widely investigated, but PI3Kγ has been

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Wolf, Z., E. Lindhoff-Last, and H. Mani. "Fortschritte in der Thrombozytenfunktionsdiagnostik." Hämostaseologie 30, no. 04 (2010): 217–29. http://dx.doi.org/10.1055/s-0037-1619053.

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SummaryBoth for diagnosis of congenital and acquired platelet dysfunction as well as for therapy monitoring after application of platelet function inhibitors various methods have been established for evaluation of platelet function. In contrast to the gold standard of platelet function testing, the light transmission aggregometry in platelet rich plasma the Point-of-care (POC) analyzers allow fast analysis of platelet function without extensive laboratory work up. The conditions of the pre-analytical phase, however, are still of enormous importance in the prevention of medical errors. There is

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Chen, Pengfei, Ying Lu, Hanchao Gao, Mingtao Li, David K. C. Cooper, and Lisha Mou. "Sequence alignment analysis of proteins involved in platelet-endothelial cell interaction identifies molecular incompatibilities between Homo sapiens and Sus scrofa." Journal of Biomedical Engineering and Informatics 3, no. 1 (2017): 51. http://dx.doi.org/10.5430/jbei.v3n1p51.

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Background: Platelets play a vital role in acute humoral xenograft rejection (AHXR) in pig-to-primate xenotransplantation, presenting as microvascular thrombosis in the graft and/or consumptive coagulopathy in the recipient. Adhesion and aggregation of primate platelets to the activated vascular endothelial cells through sequential binding of ligands on endothelial cells and subendothelial matrix ultimately trigger a complex biological process of prothrombotic signaling cascades. Increasing evidence suggests that the molecular incompatibilities in effector molecules across species may partiall

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Babić, Ivana, Mirza Bojić, Željan Maleš, et al. "Influence of flavonoids’ lipophilicity on platelet aggregation." Acta Pharmaceutica 69, no. 4 (2019): 607–19. http://dx.doi.org/10.2478/acph-2019-0040.

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Abstract Flavonoids are natural polyphenolic compounds present in a wide spectrum of plants that have a beneficial effect on human health. In the context of cardiovascular diseases related to plaque and thrombus formation, flavonoids exhibit an anti-aggregatory effect. Previously, it has been reported that all tested flavonoids exhibit an antiaggregatory effect on platelet aggregation when measured by impedance aggregometry on whole blood, in the test of aggregation induced by adenosine diphosphate (ADP). As not all flavonoids have the same targets within signaling pathways, an assumption of a

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Rock, Gail, and Maria Kolajova. "Proteomics Used To Identify the Target of a Platelet Aggregating Antibody in a Patient with HUS." Blood 104, no. 11 (2004): 852. http://dx.doi.org/10.1182/blood.v104.11.852.852.

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Abstract Hemolytic Uremic Syndrome (HUS) has considerable overlap with Thrombotic Thrombocytopenia Purpura (TTP). Recently, evidence is emerging to suggest that TTP, like HIT, is an immune mediated disorder. We have investigated the plasmas of patients with Hemolytic Uremic Syndrome to determine the presence of antibodies and the specificity of the related antigens. Methods: A 20 year old female presented with repeated episodes of HUS. She is dialysis dependent. Plasma was taken for VWF, multimers, platelet aggregation, metalloprotease and inhibitor, western blot and 2D PAGE analysis. Results:

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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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Reininger, Armin J., Markus A. Korndörfer та Laurenz J. Wurzinger. "Adhesion of ADP-activated Platelets to Intact Endothelium under Stagnation Point Flow In Vitro Is Mediated by the Integrin αIIbβ3". Thrombosis and Haemostasis 79, № 05 (1998): 998–1003. http://dx.doi.org/10.1055/s-0037-1615109.

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SummaryAs we demonstrated earlier, platelets adhere to intact endothelium provided they are activated and convectively transported against the endothelial surface. To identify the platelet receptors involved we superfused cultured endothelium with activated platelet rich plasma (PRP) by means of the Stagnation Point Flow Adhesio- Aggregometer while blocking various platelet receptors. Inhibition was performed with the tetrapeptide RGDS, the non-peptide Ro-43-8857, or a monoclonal antibody directed against integrin αIIbβ3. Platelet deposition was video-recorded and quantified by image analysis.

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Edelstein, Leonard C., Lukas M. Simon, Cory R. Lindsay, et al. "Identification of a Racially Dimorphic Variant in the Human Platelet PAR4 Thrombin Receptor Altering Platelet Function and Pharmacologic Inhibition." Blood 124, no. 21 (2014): 1434. http://dx.doi.org/10.1182/blood.v124.21.1434.1434.

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Abstract Compared to whites, blacks have a 2-fold higher incidence of coronary heart disease (CHD), and black race is an independent predictor of worse survival after CHD events after accounting for other confounding variables (e.g., socioeconomic, demographic, etc.). However, there has been a paucity of literature considering racial differences in platelet function. We recently reported results from the Platelet RNA And eXpression-1 (PRAX1) study of platelets in healthy black (n=70) and white (n=84) subjects (Edelstein et al, Nat. Med 2013). Human platelets express two thrombin receptors, pro

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