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Journal articles on the topic 'Platelet dynamics'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Dynamics of leukocyte-platelet adhesion in whole blood." Blood 78, no. 7 (1991): 1730–37. http://dx.doi.org/10.1182/blood.v78.7.1730.1730.

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Abstract The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a mar

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2

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Dynamics of leukocyte-platelet adhesion in whole blood." Blood 78, no. 7 (1991): 1730–37. http://dx.doi.org/10.1182/blood.v78.7.1730.bloodjournal7871730.

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The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a marked incre

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3

Bender, Markus, Anita Eckly, John H. Hartwig, et al. "ADF/n-cofilin–dependent actin turnover determines platelet formation and sizing." Blood 116, no. 10 (2010): 1767–75. http://dx.doi.org/10.1182/blood-2010-03-274340.

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Abstract The cellular and molecular mechanisms orchestrating the complex process by which bone marrow megakaryocytes form and release platelets remain poorly understood. Mature megakaryocytes generate long cytoplasmic extensions, proplatelets, which have the capacity to generate platelets. Although microtubules are the main structural component of proplatelets and microtubule sliding is known to drive proplatelet elongation, the role of actin dynamics in the process of platelet formation has remained elusive. Here, we tailored a mouse model lacking all ADF/n-cofilin–mediated actin dynamics in

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Wilkins, Ngozi A., Brian Storrie, and Jeffrey A. Kamykowski. "Characterization of Platelet Alpha-Granule Dynamics." Blood 116, no. 21 (2010): 327. http://dx.doi.org/10.1182/blood.v116.21.327.327.

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Abstract Abstract 327 Background: Platelets, anucleated cells that play a critical role in blood clotting, store proteins and small molecules in alpha-granules and dense granules, respectively, for secretion. Alpha-granules contain several proteins including von Willebrand factor and fibrinogen and dense granules contain serotonin. Rab4, a marker for the early endosomes has been implicated in regulating alpha granule secretions (Sirakawa et al, 2010). Previous fluorescence microscopy mapping of alpha-granule protein distributions suggested that there are either two different alpha-granule type

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Dubois, Christophe, Laurence Panicot-Dubois, Barbara C. Furie, and Bruce Furie. "Dynamics of Calcium Mobilization in Platelets during Thrombus Formation in a Living Mouse." Blood 106, no. 11 (2005): 649. http://dx.doi.org/10.1182/blood.v106.11.649.649.

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Abstract Platelet accumulation at sites of vascular injury arrests bleeding but also plays a critical role in the pathogenesis of thrombosis, leading to ischemia in myocardial infarction or stroke. Intracellular calcium mobilization in platelets is a critical step in the activation of platelets and formation of the platelet thrombus. Here we show the relationship of the dynamics of intracellular calcium mobilization with platelet accumulation into the developing thrombus in a living mouse. Following injection of 100 x 106 fura-2 loaded platelets into a living mouse we used high speed intravita

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Falet, Hervé, Gregory Chang, Brigitte Brohard-Bohn, Francine Rendu та John H. Hartwig. "Integrin αIIbβ3signals lead cofilin to accelerate platelet actin dynamics". American Journal of Physiology-Cell Physiology 289, № 4 (2005): C819—C825. http://dx.doi.org/10.1152/ajpcell.00587.2004.

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Cofilin, in its Ser3 dephosphorylated form, accelerates actin filament turnover in cells. We report here the role of cofilin in platelet actin assembly. Cofilin is primarily phosphorylated in the resting platelet as evidenced by a specific antibody directed against its Ser3 phosphorylated form. After stimulation with thrombin under nonstirring conditions, cofilin is reversibly dephosphorylated and transiently incorporates into the actin cytoskeleton. Its dephosphorylation is maximal 1–2 min after platelet stimulation, shortly after the peak of actin assembly occurs. Cofilin rephosphorylation b

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7

Patel, Dipti, Heikki Väänänen, Markéta Jiroušková, Thomas Hoffmann, Carol Bodian, and Barry S. Coller. "Dynamics of GPIIb/IIIa-mediated platelet-platelet interactions in platelet adhesion/thrombus formation on collagen in vitro as revealed by videomicroscopy." Blood 101, no. 3 (2003): 929–36. http://dx.doi.org/10.1182/blood.v101.3.929.

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Abstract The conventional description of platelet interactions with collagen-coated surfaces in vitro, based on serial static measurements, is that platelets first adhere and spread to form a monolayer and then recruit additional layers of platelets. To obtain dynamic information, we studied gravity-driven platelet deposition in vitro on purified type 1 collagen by video phase-contrast microscopy at 22°C. With untreated human and wild-type mouse platelets, soon after the initial adhesion of a small number of “vanguard” platelets, “follower” platelets attached to the spread-out vanguard platele

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8

Filipovic, N., M. Kojic, and A. Tsuda. "Modelling thrombosis using dissipative particle dynamics method." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1879 (2008): 3265–79. http://dx.doi.org/10.1098/rsta.2008.0097.

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Aim . Arterial occlusion is a leading cause of cardiovascular disease. The main mechanism causing vessel occlusion is thrombus formation, which may be initiated by the activation of platelets. The focus of this study is on the mechanical aspects of platelet-mediated thrombosis which includes the motion, collision, adhesion and aggregation of activated platelets in the blood. A review of the existing continuum-based models is given. A mechanical model of platelet accumulation onto the vessel wall is developed using the dissipative particle dynamics (DPD) method in which the blood (i.e. colloida

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Suzuki, Aae, Lurong Lian, Liang Zhao, et al. "Mice That Lack RhoA In Their Platelets Have Normal Actin Dynamics, but Have Macrothrombocytopenia." Blood 116, no. 21 (2010): 549. http://dx.doi.org/10.1182/blood.v116.21.549.549.

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Abstract Abstract 549 In response to agonist stimulation, platelets undergo a rapid reorganization of their actin cytoskeleton. This process involves simultaneous disassembly and assembly of filamentous actin, and is one of the earliest phenomena seen in platelet activation. Ex vivo flow models suggest that the platelet cytoskeleton is required for platelet adhesion that can withstand the shear conditions found within the arterial vascular system. The signaling pathways that link external stimuli with actin assembly are believed to include polyphosphoinositides, small GTP-binding proteins, and

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Patel-Hett, Sunita, Jennifer L. Richardson, Harald Schulze, et al. "Visualization of microtubule growth in living platelets reveals a dynamic marginal band with multiple microtubules." Blood 111, no. 9 (2008): 4605–16. http://dx.doi.org/10.1182/blood-2007-10-118844.

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Abstract The marginal band of microtubules maintains the discoid shape of resting blood platelets. Although studies of platelet microtubule coil structure conclude that it is composed of a single microtubule, no investigations of its dynamics exist. In contrast to previous studies, permeabilized platelets incubated with GTP-rhodamine-tubulin revealed tubulin incorporation at 7.9 (± 1.9) points throughout the coil, and anti-EB1 antibodies stained 8.7 (± 2.0) sites, indicative of multiple free microtubules. To pursue this result, we expressed the microtubule plus-end marker EB3-GFP in megakaryoc

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Haley, Kristina M., Joseph E. Aslan, Garth W. Tormoen, et al. "The PAK Signaling System Links Rho Gtpase Activation to Platelet Lamellopodia Formation, Aggregation and Aggregate Stability Under Shear." Blood 120, no. 21 (2012): 1060. http://dx.doi.org/10.1182/blood.v120.21.1060.1060.

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Abstract Abstract 1060 Platelets serve as the primary mediators of hemostasis and thrombosis, circulating as surveyors for gaps in vascular integrity. As platelets encounter exposed extracellular matrix proteins, receptors on the platelet surface trigger intracellular signaling events that result in rapid platelet activation and a complex rearrangement of platelet morphology to form filopodia and lamellipodia. Rac1, a member of the Rho GTPase family, has emerged as a key regulator in platelet actin dynamics. However, the specific downstream events following Rac1 activation that mediate platele

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Flaumenhaft, Robert C., Secil Koseoglu, James R. Dilks, et al. "Dynamin-Related Protein-1 Controls Fusion Pore Dynamics During Platelet Granule Secretion and Thrombus Formation In Vivo." Blood 118, no. 21 (2011): 361. http://dx.doi.org/10.1182/blood.v118.21.361.361.

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Abstract Abstract 361 Platelet granule secretion serves a central role in hemostasis and thrombosis. During platelet secretion, fusion of granule membranes with those of the plasma membrane results in the release of granule contents. Recently electrochemical techniques using single-cell amperometry have shown that platelet membrane fusion results in the formation of a fusion pore. The fusion pore subsequently expands to enable the complete extrusion of granule contents. However, the molecular mechanisms that control platelet fusion pore formation and expansion are not known. To discover novel

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13

JACKSON, S. P., W. S. NESBITT, and E. WESTEIN. "Dynamics of platelet thrombus formation." Journal of Thrombosis and Haemostasis 7 (July 2009): 17–20. http://dx.doi.org/10.1111/j.1538-7836.2009.03401.x.

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Tykhomyrov, A. A. "Dynamics of thrombin-induced exposition of actin on the platelet surface." Ukrainian Biochemical Journal 86, no. 5 (2014): 74–81. http://dx.doi.org/10.15407/ubj86.05.074.

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Stalker, Timothy J., Jie Wu, and Lawrence F. Brass. "Platelet Expression of a Genetically Encoded Calcium Indicator Reveals Platelet Activation Gradients in Real Time during Thrombus Formation in Vivo." Blood 124, no. 21 (2014): 96. http://dx.doi.org/10.1182/blood.v124.21.96.96.

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Abstract Introduction: Recent studies have demonstrated that platelet activation during hemostatic thrombus formation in vivo is heterogeneous in time and space. We have previously shown that in response to a penetrating injury in the microcirculation platelet accumulation and activation are driven by gradients of soluble agonists emanating from the site of injury. These gradients result in a characteristic thrombus architecture in which a core of fully activated platelets that have released their alpha granules is overlaid by a shell of less activated platelets that frequently embolize. While

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Dunne, Eimear, Qin M. Qi, Eric S. Shaqfeh, et al. "Blood group alters platelet binding kinetics to von Willebrand factor and consequently platelet function." Blood 133, no. 12 (2019): 1371–77. http://dx.doi.org/10.1182/blood-2018-06-855528.

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Abstract Blood type O is associated with a lower risk of myocardial infarction. Platelets play a critical role in myocardial infarction. It is not known whether the expression of blood group antigens on platelet proteins alters platelet function; we hypothesized that platelet function would be different between donors with blood type O and those with non-O. To address this hypothesis, we perfused blood from healthy type O donors (n = 33) or non-O donors (n = 54) over pooled plasma derived von Willebrand factor (VWF) protein and purified blood type–specific VWF at arterial shear and measured pl

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Italiano, Joseph E., Jennifer L. Richardson, Harald Schulze, et al. "The Marginal Microtubule Coil in the Resting Blood Platelet Is a Dynamic Bipolar Array." Blood 106, no. 11 (2005): 1653. http://dx.doi.org/10.1182/blood.v106.11.1653.1653.

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Abstract The discoid shape of the resting blood platelet is maintained by its marginal microtubule band. Structural studies have concluded that this band is composed of a single microtubule coiled 8-12 times around the cell periphery. To understand the dynamics of the microtubule coil, we took advantage of EB1 and EB3, proteins that highlight the ends of growing microtubules. Immunofluorescence microscopy with anti-EB1 revealed clear staining of numerous (8.7 +/− 2.0, range 4–12) comet-like dashes in the microtubule coil, suggesting the presence of several microtubule plus ends. Consistent wit

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Yu, Zhiqian, Mami Ohba, Masanori Nakamura, et al. "Dynamics of platelet mobilisation into lungs in response to 5-hydroxytryptamine (serotonin) in mice." Thrombosis and Haemostasis 102, no. 12 (2009): 1251–58. http://dx.doi.org/10.1160/th08-06-0406.

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SummaryIn experimental animals, the lung rapidly removes intravenously injected 5-hydroxytryptamine (5HT), but the mechanism underlying this pulmonary 5HT removal (P-5HT-R) and the responsible cells remains unclear. 5HT reportedly induces rapid pulmonary platelet accumulation (P-PLT-A). Here, we examined the relationship between P-5HT-R and P-PLT-A in mice by comparing the platelet count in the blood with the endogenous 5HT in the tissues (a marker for platelets because the 5HT is largely contained within platelets). 5HT levels in murine blood and tissues were also examined after intravenous i

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19

Steiner, M. "Dynamics of Platelet Tubulin in Response to Changes in Free Sulfhydryl Groups." Thrombosis and Haemostasis 53, no. 02 (1985): 176–79. http://dx.doi.org/10.1055/s-0038-1661267.

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SummaryPools of polymerized and total tubulin were measured in human platelets as a function of free sulfhydryl groups both in acid-soluble and acid-precipitable cell fractions. Changes in free thiols were produced either by storage of platelets at room temperature or by addition of the potent oxidizing agent diazene dicarboxylic acid (diamide) and were correlated with shifts in the dynamic equilibrium between assembled and disassembled microtubules and platelet aggregation. Diamide at concentrations of 0.5 to 5 mM depleted acid soluble SH groups and reduced protein thiols while causing a prog

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Vasilev, Grigorii A., Aleksandra A. Filkova, and Anastasia N. Sveshnikova. "Study of Reversible Platelet Aggregation Model by Nonlinear Dynamics." Mathematics 9, no. 7 (2021): 759. http://dx.doi.org/10.3390/math9070759.

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Blood cell platelets form aggregates upon vessel wall injury. Under certain conditions, a disintegration of the platelet aggregates, called “reversible aggregation”, is observed in vitro. Previously, we have proposed an extremely simple (two equations, five parameters) ordinary differential equation-based mathematical model of the reversible platelet aggregation. That model was based on mass-action law, and the parameters represented probabilities of platelet aggregate formations. Here, we aimed to perform a nonlinear dynamics analysis of this mathematical model to derive the biomedical meanin

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21

Hubbard, William Brad, Meenakshi Banerjee, Hemendra Vekaria, et al. "Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury." Cells 10, no. 3 (2021): 500. http://dx.doi.org/10.3390/cells10030500.

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Traumatic brain injury (TBI) affects over 3 million individuals every year in the U.S. There is growing appreciation that TBI can produce systemic modifications, which are in part propagated through blood–brain barrier (BBB) dysfunction and blood–brain cell interactions. As such, platelets and leukocytes contribute to mechanisms of thromboinflammation after TBI. While these mechanisms have been investigated in experimental models of contusion brain injury, less is known regarding acute alterations following mild closed head injury. To investigate the role of platelet dynamics and bioenergetics

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Stritt, Simon, Sarah Beck, Isabelle C. Becker, et al. "Twinfilin 2a regulates platelet reactivity and turnover in mice." Blood 130, no. 15 (2017): 1746–56. http://dx.doi.org/10.1182/blood-2017-02-770768.

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Key Points Deficiency in twinfilin 2a causes macrothrombocytopenia and hyperreactivity of platelets in mice. We provide the first in vivo evidence for an inhibitory function of twinfilin 2a in platelet actin dynamics.

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Vyshynska, M. B. "Changes in the functional state of platelets in patients with polytrauma." EMERGENCY MEDICINE 17, no. 1 (2021): 27–32. http://dx.doi.org/10.22141/2224-0586.17.1.2021.225716.

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Background. Polytrauma remains the leading cause of global morbidity and mortality and is the cause of more than 10 % of deaths. The purpose of this research was to study the literature data about changes in vascular platelet hemostasis, to investigate the dynamics of the morphofunctional state of platelets, to analyze changes in intravascular platelet activation in patients with polytrauma. Results. Normal blood clotting requires at least 4 components — blood vessels, platelets, the ability of blood to coagulate and fibrinolysis. Determination of components such as indicators of intravascula

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Pula, Giordano, Kai Schuh, Keiko Nakayama, Keiichi I. Nakayama, Ulrich Walter та Alastair W. Poole. "PKCδ regulates collagen-induced platelet aggregation through inhibition of VASP-mediated filopodia formation". Blood 108, № 13 (2006): 4035–44. http://dx.doi.org/10.1182/blood-2006-05-023739.

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Abstract Protein kinase Cδ (PKCδ) has been shown by pharmacologic approaches to negatively regulate collagen-induced platelet aggregation. Here we addressed the molecular and cellular mechanisms underlying this negative regulation. Using PKCδ–/– platelets, we show that the mechanism did not involve altered inside-out signaling to integrin αIIbβ3 and did not affect early signaling events downstream of GPVI, because there was no difference in tyrosine phosphorylation of PLCγ2 between wild-type and PKCδ–/– platelets. There was also no increase in secretion of dense granule content, in contrast to

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Tauber, Helmuth, Nicole Innerhofer, Daniel von Langen, et al. "Dynamics of Platelet Counts in Major Trauma: The Impact of Haemostatic Resuscitation and Effects of Platelet Transfusion—A Sub-Study of the Randomized Controlled RETIC Trial." Journal of Clinical Medicine 9, no. 8 (2020): 2420. http://dx.doi.org/10.3390/jcm9082420.

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Although platelets play a central role in haemostasis, the dynamics of platelet counts during haemostatic resuscitation, the response to platelet transfusion, and effects on clinical outcome are poorly described for trauma patients. As a sub-study of the already published randomized controlled RETIC Study “Reversal of Trauma-induced Coagulopathy using First-line Coagulation Factor Concentrates or Fresh-Frozen Plasma” trial, we here analysed whether the type of first-line haemostatic resuscitation influences the frequency of platelet transfusion and determined the effects of platelet transfusio

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de Vrij, Edwin L., Hjalmar R. Bouma, Maaike Goris, et al. "Reversible thrombocytopenia during hibernation originates from storage and release of platelets in liver sinusoids." Journal of Comparative Physiology B 191, no. 3 (2021): 603–15. http://dx.doi.org/10.1007/s00360-021-01351-3.

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AbstractImmobility is a risk factor for thrombosis due to low blood flow, which may result in activation of the coagulation system, recruitment of platelets and clot formation. Nevertheless, hibernating animals—who endure lengthy periods of immobility—do not show signs of thrombosis throughout or after hibernation. One of the adaptations of hemostasis in hibernators consists of a rapidly reversible reduction of the number of circulating platelets during torpor, i.e., the hibernation phase with reduction of metabolic rate, low blood flow and immobility. It is unknown whether these platelet dyna

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Nikolaieva, I., T. Halenova, and O. Savchuk. "Modern concepts of the role of platelet receptors in the dynamics of thrombus formation." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 70, no. 2 (2015): 5–11. http://dx.doi.org/10.17721/1728_2748.2015.70.5-11.

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The study of molecular and biological aspects of the platelets functioning with the use of biochemical methods, new technologies of cell and molecular biology became the basis for understanding signaling cascades regulating the activation, adhesion and aggregation of these cells. In this review, the general modern information of the role of platelet membrane receptors in physiological and pathological processes of thrombus formation was performed. The possible role of platelet receptors as target of antiagregatory agents was analyzed. Also, new promising areas of searching for effective and sp

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Stritt, Simon, Inga Birkholz, Sarah Beck, et al. "Profilin 1–mediated cytoskeletal rearrangements regulate integrin function in mouse platelets." Blood Advances 2, no. 9 (2018): 1040–45. http://dx.doi.org/10.1182/bloodadvances.2017014001.

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Key Points Profilin 1–mediated cytoskeletal dynamics regulate platelet β1- and β3-integrin function and turnover. Profilin 1 deficiency in platelets impairs hemostasis and results in a marked protection from arterial thrombosis.

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Stefanich, Eric, Tauri Senn, Ramon Widmer, Christine Fratino, Gilbert-André Keller, and Paul J. Fielder. "Metabolism of Thrombopoietin (TPO) In Vivo: Determination of the Binding Dynamics for TPO in Mice." Blood 89, no. 11 (1997): 4063–70. http://dx.doi.org/10.1182/blood.v89.11.4063.

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AbstractPrevious in vivo studies have established that plasma thrombopoietin (TPO) levels are regulated by binding to c-Mpl on platelets and that, in vitro, platelets bind and degrade TPO. To determine if the in vivo metabolism of TPO was specific and saturable, we injected normal CD-1 mice IV with trace amounts of 125I-rmTPO with or without a saturating concentration of rmTPO. The amount of radioactivity present in the spleen, blood cell fraction, platelet fraction, tibia/fibula, and femur was significantly greater in the mice receiving 125I-rmTPO alone. Conversely, the amount of radioactivit

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Babur, Özgün, Anh T. P. Ngo, Rachel A. Rigg, et al. "Platelet procoagulant phenotype is modulated by a p38-MK2 axis that regulates RTN4/Nogo proximal to the endoplasmic reticulum: utility of pathway analysis." American Journal of Physiology-Cell Physiology 314, no. 5 (2018): C603—C615. http://dx.doi.org/10.1152/ajpcell.00177.2017.

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Upon encountering physiological cues associated with damaged or inflamed endothelium, blood platelets set forth intracellular responses to ultimately support hemostatic plug formation and vascular repair. To gain insights into the molecular events underlying platelet function, we used a combination of interactome, pathway analysis, and other systems biology tools to analyze associations among proteins functionally modified by reversible phosphorylation upon platelet activation. While an interaction analysis mapped out a relative organization of intracellular mediators in platelet signaling, pa

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Dopheide, Sacha M., Mhairi J. Maxwell, and Shaun P. Jackson. "Shear-dependent tether formation during platelet translocation on von Willebrand factor." Blood 99, no. 1 (2002): 159–67. http://dx.doi.org/10.1182/blood.v99.1.159.

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The adhesion and aggregation of platelets at sites of vascular injury is dependent on the initial binding of the GP Ib/V/IX receptor complex to immobilized von Willebrand factor (VWF). Under flow conditions, this interaction supports platelet translocation that is characteristically stop-start in nature. High resolution imaging of platelets during surface translocation on immobilized VWF revealed that thin membrane tethers (length: 0.91 μm-47.90 μm) were pulled from the surface of these cells. Membrane tethers were dynamic structures that extended from small, localized adhesion contacts under

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Kim, Dongjune A., Katrina J. Ashworth, Jorge Di Paola та David N. Ku. "Platelet α-granules are required for occlusive high-shear-rate thrombosis". Blood Advances 4, № 14 (2020): 3258–67. http://dx.doi.org/10.1182/bloodadvances.2020002117.

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Abstract von Willebrand factor (VWF) is essential for the induction of arterial thrombosis. In this study, we investigated the critical role of platelet VWF in occlusive thrombosis formation at high shear in mice that do not express platelet VWF (Nbeal2−/−). Using in silico modeling, in vitro high-shear microfluidics, and an in vivo Folts model of arterial thrombosis we reproduced the platelet dynamics that occur under pathological flow in a stenosed vessel. Computational fluid dynamics (CFDs) simulated local hemodynamics in a stenosis based on arterial geometries. The model predicted shear ra

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Sakurai, Yumiko, David R. Myers, Ashley Kita, and Wilbur Lam. "A Novel Assay That Integrates the Effects of Multiple Agonists At the Single-Platelet Level,." Blood 118, no. 21 (2011): 3258. http://dx.doi.org/10.1182/blood.v118.21.3258.3258.

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Abstract Abstract 3258 Background: At sites of vascular injury, platelets are exposed to multiple agonists that lead to overall activation and platelet plug formation. Signaling pathways induced by these agonists are known to interact with each other. For example, collagen binding to the platelet collagen receptors, α2β1 integrin, CD36, and glycoprotein VI, induces inside-out signaling that ultimately leads to the activation of the glycoprotein IIb/IIIa receptor for fibrinogen on the platelet surface (Nakamura et al, JCB, 1999). An assay capable of tracking the biological effects of multiple d

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Lorenz, Martin, Herbert Merk, Michael Buchanan, Wolfgang Eisert, and Joanne van Ryn. "Accumulation of radiolabelled platelets and fibrin on the carotid artery of rabbits after angioplasty: effects of heparin and dipyridamole." Thrombosis and Haemostasis 90, no. 12 (2003): 1179–86. http://dx.doi.org/10.1160/th03-05-0305.

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SummaryWe investigated the dynamic accumulation of platelets and fibrin after balloon injury of the carotid arteries in rabbits in vivo. In addition, effects of heparin and dipyridamole treatment were also tested. Autologous 99mTc-labelled platelet and 123I-labelled fibrin accumulation was measured at one minute intervals for 4 hours following balloon injury of the carotid artery. Platelet accumulation occurred rapidly, with a ~125% increase occurring within 30 min after injury. There was no further activity for up to 4 hours. This accumulation could be inhibited with an intravenous infusion o

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Wang, Yanfeng, Aae Suzuki, Lurong Lian та ін. "Platelets Lacking PIP5KIγ Have Impaired Cytoskeletal Dynamics and Adhesion, but No Defect in Integrin Activation." Blood 114, № 22 (2009): 772. http://dx.doi.org/10.1182/blood.v114.22.772.772.

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Abstract Abstract 772 Following thrombin stimulation, platelet PIP5KI synthesizes phosphatidylinositol 4,5-bisphosphate (PIP2), which can be hydrolyzed by phospholipase C to generate second messengers such as IP3. PIP2 also regulates cytoskeletal dynamics by directly interacting with actin-binding proteins such as talin. Three isoforms of PIP5KI (α, β, and γ) are all capable of phosphorylating PI4P to synthesize PIP2. We have generated and characterized murine lines lacking individual PIP5KI isoforms. While mice lacking PIP5KIα and PIP5KIα have absent second messenger formation and partially i

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Emel’yanova, A. N., and Yu A. Vitkovskiy. "Lymphocyte-platelet adhesion and aggregation of platelets in patients with erysipelas." Kazan medical journal 93, no. 2 (2012): 216–20. http://dx.doi.org/10.17816/kmj2292.

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Aim. To study the lymphocyte-platelet adhesion in patients with various forms of erysipelas in the dynamics of treatment. Methods. 90 patients with erysipelas participated in the study: 20 with the erythematous-bullous form and 20 with the erythematous form. According to the recurrence of the disease the patients were divided into two groups: the main group (40 patients with the primary form of erysipelas) and the comparison group (50 people with recurrent erysipelas). The control group, which was comparable by sex and age, was comprised of 55 healthy people. The index of lymphocyte-platelet a

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Savolainen, S., M. T. Syrjälä, K. Liewendahl, J. Gripenberg, and U. Nieminen. "Compartmental analysis of short-lived platelet dynamics." Scandinavian Journal of Clinical and Laboratory Investigation 50, no. 6 (1990): 679–86. http://dx.doi.org/10.3109/00365519009089187.

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Dragnea, Elena-Mihaela. "The dynamics of platelet volume in sepsis." Journal of Contemporary Clinical Practice 2, no. 2 (2016): 75–76. http://dx.doi.org/10.18683/jccp.2016.1016.

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39

Vignesh, Pandiarajan, and Surjit Singh. "Platelet Activation Dynamics in Kawasaki Disease– Revisited." Indian Journal of Pediatrics 86, no. 3 (2019): 216–17. http://dx.doi.org/10.1007/s12098-019-02890-y.

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Lee, Dooyoung, Karen P. Fong, Michael R. King, Lawrence F. Brass, and Daniel A. Hammer. "Differential Dynamics of Platelet Contact and Spreading." Biophysical Journal 102, no. 3 (2012): 472–82. http://dx.doi.org/10.1016/j.bpj.2011.10.056.

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41

Tesakov, I. P., A. A. Martyanov, A. E. Drui, and A. N. Sveshnikova. "Analysis of platelet RNA: a non-invasive method for studying the expression of tumor genes." Pediatric Hematology/Oncology and Immunopathology 20, no. 1 (2021): 207–17. http://dx.doi.org/10.24287/1726-1708-2021-20-1-207-217.

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Nowadays much attention is paid to non-invasive methods of cancer diagnostics and monitoring. One of the promising methods is the sequencing of platelet RNA (tumor-educated platelets), in which, as it was previously established, the mRNA repertoire changes in various oncological diseases. Thus, platelets can contain information about the molecular genetic characteristics of tumor. This review summarizes the current understanding of the mechanisms of interaction between tumor cells and platelets, and also discusses the possibilities of using platelet transcriptome analysis methods for diagnosin

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42

Horev, Melanie B., Yishaia Zabary, Revital Zarka, et al. "Differential dynamics of early stages of platelet adhesion and spreading on collagen IV- and fibrinogen-coated surfaces." F1000Research 9 (May 27, 2020): 449. http://dx.doi.org/10.12688/f1000research.23598.1.

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Background: Upon wound formation, platelets adhere to the neighboring extracellular matrix and spread on it, a process which is critical for physiological wound healing. Multiple external factors, such as the molecular composition of the environment and its mechanical properties, play a key role in this process and direct its speed and outcome. Methods: We combined live cell imaging, quantitative interference reflection microscopy and cryo-electron tomography to characterize, at a single platelet level, the differential spatiotemporal dynamics of the adhesion process to fibrinogen- and collage

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43

Horev, Melanie B., Yishaia Zabary, Revital Zarka, et al. "Differential dynamics of early stages of platelet adhesion and spreading on collagen IV- and fibrinogen-coated surfaces." F1000Research 9 (July 3, 2020): 449. http://dx.doi.org/10.12688/f1000research.23598.2.

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Background: Upon wound formation, platelets adhere to the neighboring extracellular matrix and spread on it, a process which is critical for physiological wound healing. Multiple external factors, such as the molecular composition of the environment and its mechanical properties, play a key role in this process and direct its speed and outcome. Methods: We combined live cell imaging, quantitative interference reflection microscopy and cryo-electron tomography to characterize, at a single platelet level, the differential spatiotemporal dynamics of the adhesion process to fibrinogen- and collage

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44

Tablin, Fern, and John H. Crowe. "Human Platelet Membrane Lipid Dynamics: Agonist Stimulation Results in the Aggregation of Lipid Rafts and the Lateral Phase Separation of like Lipids in Intact Human Platelets." Blood 104, no. 11 (2004): 3530. http://dx.doi.org/10.1182/blood.v104.11.3530.3530.

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Abstract Sphingomyelin and cholesterol rich platelet membrane domains are organized into lipid rafts, which are present in the liquid ordered state, and which have been suggested to be key membrane components both during cold-induced human platelet activation (Gousset et al. 2002 Evidence for a physiological role for membrane rafts in human platelets. J. Cellular Physiol. 190:117–128) as well as during agonist induced activation. We have previous demonstrated that platelets have two membrane phase transitions, a raft transition at 34–40°C (Gousset et al., 2002 ) and a phospholipid phase transi

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45

Yangfan Zhou, Mengjiao Hu, Xiaoyan Chen та ін. "Migfilin supports hemostasis and thrombosis through regulating platelet αIIbβ3 outside-in signaling." Haematologica 105, № 11 (2019): 2608–18. http://dx.doi.org/10.3324/haematol.2019.232488.

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Elucidating the regulation mechanism of integrin αIIbβ3 is key to understand platelet biology and thrombotic diseases. Previous in vitro studies have implicated a role of migfilin in the support of platelet αIIbβ3 activation, however, contribution of migfilin to thrombosis and hemostasis in vivo and a detailed mechanism of migfilin in platelets are not known. In this study, with migfilin deletion (migfilin-/-) mice, we report that migfilin is a pivotal positive regulator of hemostasis and thrombosis. Migfilin-/- mice showed a nearly doubled tail-bleeding time and a prolonged occlusion time in

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Gill, J., C. S. Thompson, J. Y. Jeremy, and D. P. Mikhailidis. "Adrenoceptor-linked [45Ca2+] uptake in platelets from diabetic rats: a model for human platelets." Laboratory Animals 28, no. 2 (1994): 143–47. http://dx.doi.org/10.1258/002367794780745326.

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Adrenoceptor-linked 45calcium uptake was investigated in platelets from diabetic rats (hyperglycaemic, streptozotocin-induced, of 60 days duration). Basal uptake was markedly enhanced in platelets from diabetic rats compared with controls. However, whereas adrenaline-stimulated uptake was unchanged, isoprenaline-stimulated uptake was significantly reduced and noradrenaline-stimulated uptake significantly increased. These latter data indicate that there are differential alterations of adrenoceptor subtypes in diabetes (i.e. an increase in alpha- but decrease in beta-adrenoceptors). These change

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47

Diamond, Scott L. "Systems Biology to Predict Platelet Function." Blood 116, no. 21 (2010): SCI—38—SCI—38. http://dx.doi.org/10.1182/blood.v116.21.sci-38.sci-38.

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Abstract Abstract SCI-38 Systems Biology seeks to provide patient-specific prediction of dynamic cellular response to multiple stimuli, critical information toward predicting risk, disease progression, or response to therapy. We deployed two distinct approaches, bottom-up and top-down analyses, to gain insight into platelet signaling. The bottom-up approach required a definition of reaction network and kinetic equations (topology), kinetic parameters, and initial concentrations in order to simulate platelet signaling. We developed a computational platelet model – assembled from 24 peer-reviewe

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Lian, Lurong, Yanfeng Wang, Julia Draznin та ін. "The relative role of PLCβ and PI3Kγ in platelet activation". Blood 106, № 1 (2005): 110–17. http://dx.doi.org/10.1182/blood-2004-05-2005.

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Stimulation of platelet G protein–coupled receptors results in the cleavage of phosphatidylinositol 4,5-trisphosphate (PIP2) into inositol 1,4,5-trisphosphate and 1,2-diacylglycerol by phospholipase C (PLCβ). It also results in the phosphorylation of PIP2 by the γ isoform of phosphatidylinositol 3-kinase (PI3Kγ) to synthesize phosphatidylinositol 3,4,5-trisphosphate. To understand the role of PIP2 in platelet signaling, we evaluated knock-out mice lacking 2 isoforms of PLCβ (PLCβ2 and PLCβ3) or lacking the Gβγ-activated isoform of PI3K (PI3Kγ). Both knock-out mice were unable to form stable th

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Wiśniewski, Adam, Joanna Sikora, Aleksandra Karczmarska-Wódzka, Joanna Bugieda, Karolina Filipska, and Robert Ślusarz. "Unfavorable Dynamics of Platelet Reactivity during Clopidogrel Treatment Predict Severe Course and Poor Clinical Outcome of Ischemic Stroke." Brain Sciences 11, no. 2 (2021): 257. http://dx.doi.org/10.3390/brainsci11020257.

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Background: Previous studies have revealed that high platelet reactivity while on clopidogrel may affect the severe course and worse prognosis of ischemic stroke. However, the above findings were based on a single measurement of platelet function. We aimed to investigate whether the dynamics of platelet reactivity over time would more accurately determine its actual impact on clinical outcome. Methods: We enrolled 74 ischemic stroke subjects, taking a dose of 75 mg a day of clopidogrel to this prospective, single-center, and observational study. The determination of platelet function was based

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Mody, Nipa A., and Michael R. King. "Platelet Adhesive Dynamics. Part I: Characterization of Platelet Hydrodynamic Collisions and Wall Effects." Biophysical Journal 95, no. 5 (2008): 2539–55. http://dx.doi.org/10.1529/biophysj.107.127670.

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