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Journal articles on the topic 'Platelet function'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Stolla, Moritz, Renata Grozovsky, Melissa M. Lee-Sundlov, Herve Falet, and Karin M. Hoffmeister. "Effects of Platelet Circulatory Age on Platelet Function." Blood 128, no. 22 (2016): 413. http://dx.doi.org/10.1182/blood.v128.22.413.413.

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Abstract The human body produces and removes 1011 platelets daily to maintain a normal steady-state platelet count. However, the regulatory mechanisms remain elusive. We have shown that platelets lacking sialic acid (desialylated platelets) are removed by the hepatic Ashwell-Morell receptor (AMR or asialoglycoprotein receptor type 2), thereby regulating platelet survival and hepatic TPO levels. Platelet counts and lifetime were increased in Asgr2-/- mice (AMR-null mice), compared to wild type (WT) mice. Platelet volume and immature platelet fraction (IPF) are decreased in AMR-null mice, consis

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Coxon, Carmen H., Alexander M. Lewis, Amanda J. Sadler, et al. "NAADP regulates human platelet function." Biochemical Journal 441, no. 1 (2011): 435–42. http://dx.doi.org/10.1042/bj20111175.

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Platelets play a vital role in maintaining haemostasis. Human platelet activation depends on Ca2+ release, leading to cell activation, granule secretion and aggregation. NAADP (nicotinic acid–adenine dinucleotide phosphate) is a Ca2+-releasing second messenger that acts on acidic Ca2+ stores and is used by a number of mammalian systems. In human platelets, NAADP has been shown to release Ca2+ in permeabilized human platelets and contribute to thrombin-mediated platelet activation. In the present study, we have further characterized NAADP-mediated Ca2+ release in human platelets in response to

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3

Margraf, Andreas, Claudia Nussbaum, and Markus Sperandio. "Ontogeny of platelet function." Blood Advances 3, no. 4 (2019): 692–703. http://dx.doi.org/10.1182/bloodadvances.2018024372.

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AbstractAlthough the hemostatic potential of adult platelets has been investigated extensively, regulation of platelet function during fetal life is less clear. Recent studies have provided increasing evidence for a developmental control of platelet function during fetal ontogeny. Fetal platelets feature distinct differences in reactive properties compared with adults. These differences very likely reflect a modified hemostatic and homeostatic environment in which platelet hyporeactivity contributes to prevent pathological clot formation on the one hand but still ensures sufficient hemostasis

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Feng, Shuju, Michael H. Kroll, Alpa M. Nick, Anil Sood, and Vahid Afshar-Kharghan. "Platelet Function in Ovarian Cancer." Blood 126, no. 23 (2015): 4656. http://dx.doi.org/10.1182/blood.v126.23.4656.4656.

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Abstract A significant number of patients with ovarian cancer develop venous thromboembolism that is associated with a worse prognosis. The etiology of an increased frequency of venous thrombosis in cancer patients is not clear, and various hypotheses, including the presence of hyperreactive platelets, have been postulated. Hyperreactive platelets have a lower threshold for aggregation, and hence there is a higher number of degranulated platelets in circulation and a higher concentration of platelet granular contents in plasma. We compared ADP- and collagen-induced platelet aggregation in pati

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Iwaszko-Simonik, A., and S. Graczyk. "Evaluation of platelet function in horses undergoing colic surgery using the PFA-100 platelet function analyser." Veterinární Medicína 60, No. 9 (2016): 476–82. http://dx.doi.org/10.17221/8438-vetmed.

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6

Fidler, Trevor P., Jesse W. Rowley, Claudia Araujo, et al. "Superoxide Dismutase 2 is dispensable for platelet function." Thrombosis and Haemostasis 117, no. 10 (2017): 1859–67. http://dx.doi.org/10.1160/th17-03-0174.

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SummaryIncreased intracellular reactive oxygen species (ROS) promote platelet activation. The sources of platelet-derived ROS are diverse and whether or not mitochondrial derived ROS, modulates platelet function is incompletely understood. Studies of platelets from patients with sickle cell disease, and diabetes suggest a correlation between mitochondrial ROS and platelet dysfunction. Therefore, we generated mice with a platelet specific knockout of superoxide dismutase 2 (SOD2-KO) to determine if increased mitochondrial ROS increases platelet activation. SOD2-KO platelets demonstrated decreas

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Sloand, J. A., and E. M. Sloand. "Studies on platelet membrane glycoproteins and platelet function during hemodialysis." Journal of the American Society of Nephrology 8, no. 5 (1997): 799–803. http://dx.doi.org/10.1681/asn.v85799.

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Hemodialysis only partially corrects the defects in platelet function associated with uremia. Platelet contact with the artificial surfaces of the dialysis filter during hemodialysis can itself cause platelet activation, degranulation, and loss of platelet membrane glycoproteins. Although the transient platelet dysfunction that occurs after platelet contact with foreign surfaces during cardiopulmonary bypass has been well characterized, there has been no such investigation of hemodialysis. In this study of hemodialysis patients, bleeding times (BT) and the response of their platelets to thromb

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8

Coughlin, Shaun. "Protease-Activated Receptors and Platelet Function." Thrombosis and Haemostasis 82, no. 08 (1999): 353–56. http://dx.doi.org/10.1055/s-0037-1615853.

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IntroductionPlatelet activation is critical for normal hemostasis, and platelet-dependent arterial thrombosis underlies most myocardial infarctions. Thrombin is the most potent activator of platelets.1,2 For this reason, understanding the process by which thrombin activates platelets is necessary for understanding hemostasis and thrombosis and may yield novel anti-platelet therapies. This chapter focuses on our recent studies of the receptors that mediate activation of human platelets by thrombin.3,4 Thrombin signaling is mediated, at least in part, by a family of G protein-coupled protease-ac

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9

Mongirdienė, Aušra. "Possibilities of platelet function assays." Medicina 43, no. 10 (2007): 767. http://dx.doi.org/10.3390/medicina43100098.

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The aim of this article is to review various methods used and started to introduce into practice for determining platelet function, their possibilities, advantages, and disadvantages. Nowadays, in platelet function investigations, devices and their systems with unequal possibilities, operating in different principles, are used. However, because of a wide variety of platelets defects, none of them gives the accuracy of 100%. In order to avoid mistakes, several assays are used. Analysis of platelets function testing is represented in two ways: according to its investigation object and investigat

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10

Flaumenhaft, Robert, James R. Dilks, and Derek S. Sim. "Protein Palmitoylation in Platelet Function: Role in G Protein-Mediated Platelet Activation and Platelet Recruitment into Thrombi." Blood 106, no. 11 (2005): 650. http://dx.doi.org/10.1182/blood.v106.11.650.650.

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Abstract Protein palmitoylation represents the covalent linkage of a 16-carbon saturated fatty acid to a protein. This reversible post-translational modification directs protein-protein interactions as well as protein association with membranes and lipid rafts. Protein palmitoylation participates in ligand-induced signal transduction in several nucleated cells. Its role in platelet activation, however, has not previously been evaluated. We have found that platelets contain the palmitoyl transfer proteins GODZ and HIP14 as well as the palmitoyltransferase, acyl-protein thioesterase 1 (APT1). Th

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11

Brass, Lawrence. "Understanding and Evaluating Platelet Function." Hematology 2010, no. 1 (2010): 387–96. http://dx.doi.org/10.1182/asheducation-2010.1.387.

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Abstract The contribution of platelets to normal hemostasis and vascular disease is well described. However, recent studies make it clear that much remains to be learned about platelet activation at the single cell and the molecular level, and about the contribution of platelets to inflammation, tumor angiogenesis, and embryonic development. This article is divided into two themes. The first is an overview of current knowledge of the mechanisms that drive platelet function in vivo and a brief summary of some of the emerging ideas that are modifying older views. The second theme is a considerat

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Dangwal, Seema, and Thomas Thum. "MicroRNAs in platelet biogenesis and function." Thrombosis and Haemostasis 108, no. 10 (2012): 599–604. http://dx.doi.org/10.1160/th12-03-0211.

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SummaryPlatelets are important to maintain primary haemostasis and play a key role in pathology of thrombotic and occlusive vascular disorders such as acute coronary syndrome or stroke. Despite of lacking a nucleus and genomic DNA, platelets possess diverse types of RNAs, ranging from protein coding messenger RNAs to small non-coding RNAs inherited from their parent megakaryocytes. Indeed, platelets are capable of using their own translational machinery to synthesise proteins upon their activation suggesting the possibility of post-transcriptional gene regulation in platelets. MicroRNAs (miRNA

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13

Sørensen, Anne Louise, Viktoria Rumjantseva, Sara Nayeb-Hashemi, et al. "Role of Sialic Acid for Platelet Lifespan and Function." Blood 112, no. 11 (2008): 2864. http://dx.doi.org/10.1182/blood.v112.11.2864.2864.

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Abstract Although sialic acid is considered a key determinant for the survival of circulating blood cells and glycoproteins, its role in platelet half-life is not fully clarified. We and others have previously provided evidence that thrombocytopenia in mice deficient in the ST3Gal-IV sialyltransferase gene (ST3Gal-IV−/− mice) is caused by rapid clearance of the platelets due to recognition of surface galactose by asialoglycoprotein receptor-expressing scavenger cells. Here we report new insight into clearance mechanisms, activation and production of sialic acid deficient platelets. Immunofluor

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Sturm, Alexander, Helge Hebestreit, and Ralf Grossmann. "Platelet Proinflammatory and Hemostatic Function Is Differentially Regulated in Cystic Fibrosis." Blood 108, no. 11 (2006): 3948. http://dx.doi.org/10.1182/blood.v108.11.3948.3948.

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Abstract Introduction: Platelet function and mechanisms of platelet-leukocyte interactions have been investigated in several vascular und inflammatory disorders. In most studies, platelet activation and an increase of platelet-leukocyte-aggregates (PLA) could be observed. We investigated platelet function in clinically stable patients with cystic fibrosis (CF). Methods: In addition to routine markers of inflammation (e. g. CRP, IgG, ESR) parameters of platelet function were measured in 54 clinically stable CF patients and 55 healthy controls (age range 3 to 41 years): The percentage of P-selec

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15

Lu, Jun, Peng Hu, Guangyu Wei, Qi Luo, Jianlin Qiao, and Deqin Geng. "Effect of alteplase on platelet function and receptor expression." Journal of International Medical Research 47, no. 4 (2019): 1731–39. http://dx.doi.org/10.1177/0300060519829991.

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Objective To investigate the role of alteplase, a widely-used thrombolytic drug, in platelet function. Methods Human platelets were incubated with different concentrations of alteplase followed by analysis of platelet aggregation in response to adenosine diphosphate (ADP), collagen, ristocetin, arachidonic acid or epinephrine using light transmittance aggregometry. Platelet activation and surface levels of platelet receptors GPIbα, GPVI and αIIbβ3 were analysed using flow cytometry. The effect of alteplase on clot retraction was also examined. Results This study demonstrated that alteplase sig

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16

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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17

Prudent, Michel. "What about Platelet Function in Platelet Concentrates?" Hämostaseologie 40, no. 04 (2020): 500–508. http://dx.doi.org/10.1055/a-1210-3229.

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AbstractThe characterization of platelet concentrates (PCs) in transfusion medicine has been performed with different analytical methods and platelet lesions (from biochemistry to cell biology) have been documented. In routine quality assessment and validation of manufacturing processes of PCs for transfusion purposes, only basic parameters are monitored and the platelet functions are not included. However, PCs undergo several manipulations during the processing and the basic parameters do not provide sensitive analyses to properly picture out the impact of the blood component preparation and

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18

Jurk, K. "Analysis of platelet function and dysfunction." Hämostaseologie 35, no. 01 (2015): 60–72. http://dx.doi.org/10.5482/hamo-14-09-0047.

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SummaryAlthough platelets act as central players of haemostasis only their cross-talk with other blood cells, plasma factors and the vascular compartment enables the formation of a stable thrombus. Multiple activation processes and complex signalling networks are responsible for appropriate platelet function. Thus, a variety of platelet function tests are available for platelet research and diagnosis of platelet dysfunction. However, universal platelet function tests that are sensitive to all platelet function defects do not exist and therefore diagnostic algorithms for suspected platelet func

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19

Lowenstein, Charles J. "Nitric Oxide and Platelet Function." Blood 112, no. 11 (2008): sci—50—sci—50. http://dx.doi.org/10.1182/blood.v112.11.sci-50.sci-50.

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Abstract Nitric Oxide (NO) is a versatile messenger molecule of the vascular system. Three different NO synthase (NOS) isoforms found in the vasculature can synthesize NO: endothelial NOS, neuronal NOS, and inducible NOS. Once produced, NO can diffuse across cell membranes and modulate the cell biology of leukocytes, endothelial cells, and platelets. NO has several classes of molecular targets, including proteins with heme moieties, such as guanyly cyclase, cysteine residues of proteins, and radicals, such as superoxide. NO influences platelets through at least two distinct pathways. NO activa

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Reininger, A. J. "Platelet function under high shear conditions." Hämostaseologie 29, no. 01 (2009): 21–24. http://dx.doi.org/10.1055/s-0037-1616934.

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SummaryBlood platelets are the first line of defense against bleeding and as such involved in the haemostatic repair of damaged vasculature. Their true prowess seems to be displayed under high shear conditions where platelets interact with a variety of plasma proteins, all of which are tightly regulated to close the leak but at the same time prevent lumen occlusion and thromboembolism. The first task is to arrest fast flowing platelets on exposed collagen of the damaged subendothelial surface. Although platelets are endowed with several collagen receptors, most notably integrin ╒2b®1 and the i

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21

Gordy, Dominique, and Elizabeth Stone. "Mouse Model for Platelet Aggregation using Flow Cytometry." American Journal of Clinical Pathology 158, Supplement_1 (2022): S8—S9. http://dx.doi.org/10.1093/ajcp/aqac126.014.

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Abstract Platelets play crucial roles in hemostasis, bleeding, and thrombosis. Within the United States, an estimated 7,000 platelet units are transfused daily. The gold standard to measure platelet survival in humans is to determine post-transfusion recovery after an autologous transfusion of radiolabeled platelet units, however, the ability to detect platelets circulating after transfusion does not provide information on how well these platelets function in hemostasis. Clinically, platelet unit function is routinely measured using aggregometry, which requires large volumes of platelet concen

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22

Montenont, Emilie, Seema Bhatlekar, Shancy Jacob, et al. "CRISPR-edited megakaryocytes for rapid screening of platelet gene functions." Blood Advances 5, no. 9 (2021): 2362–74. http://dx.doi.org/10.1182/bloodadvances.2020004112.

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Abstract Human anucleate platelets cannot be directly modified using traditional genetic approaches. Instead, studies of platelet gene function depend on alternative models. Megakaryocytes (the nucleated precursor to platelets) are the nearest cell to platelets in origin, structure, and function. However, achieving consistent genetic modifications in primary megakaryocytes has been challenging, and the functional effects of induced gene deletions on human megakaryocytes for even well-characterized platelet genes (eg, ITGA2B) are unknown. Here we present a rapid and systematic approach to scree

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23

Shevchuk, Olga, Antonija Jurak Begonja, Stepan Gambaryan, et al. "Proteomics: A Tool to Study Platelet Function." International Journal of Molecular Sciences 22, no. 9 (2021): 4776. http://dx.doi.org/10.3390/ijms22094776.

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Platelets are components of the blood that are highly reactive, and they quickly respond to multiple physiological and pathophysiological processes. In the last decade, it became clear that platelets are the key components of circulation, linking hemostasis, innate, and acquired immunity. Protein composition, localization, and activity are crucial for platelet function and regulation. The current state of mass spectrometry-based proteomics has tremendous potential to identify and quantify thousands of proteins from a minimal amount of material, unravel multiple post-translational modifications

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24

Haining, Elizabeth J., Jing Yang, and Michael G. Tomlinson. "Tetraspanin microdomains: fine-tuning platelet function." Biochemical Society Transactions 39, no. 2 (2011): 518–23. http://dx.doi.org/10.1042/bst0390518.

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Platelets are crucial for preventing excessive blood loss at sites of injury by plugging holes in damaged blood vessels through thrombus formation. Platelet thrombi can, however, cause heart attack or stroke by blocking diseased vessels upon rupture of atherosclerotic plaques. Current anti-platelet therapy is not effective in all patients and carries a risk of bleeding. As such, a major goal in platelet research is to identify new drug targets to specifically inhibit platelets in disease processes. Tetraspanins are potential candidates because of their capacity to regulate other proteins in mi

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Solomon, Cristina, Stefan Traintinger, Bernhard Ziegler, et al. "Platelet function following trauma." Thrombosis and Haemostasis 106, no. 08 (2011): 322–30. http://dx.doi.org/10.1160/th11-03-0175.

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SummaryPlatelets play a central role in coagulation. Currently, information on platelet function following trauma is limited. We performed a retrospective analysis of patients admitted to the emergency room (ER) at the AUVA Trauma Centre, Salzburg, after sustaining traumatic injury. Immediately after admission to the ER, blood was drawn for blood cell counts, standard coagulation tests, and platelet function testing. Platelet function was assessed by multiplate electrode aggregometry (MEA) using adenosine diphosphate (ADPtest), collagen (COLtest) and thrombin receptor activating peptide-6 (TRA

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Henry, Raymond. "Platelet Function." Seminars in Thrombosis and Hemostasis 4, no. 02 (2008): 93–122. http://dx.doi.org/10.1055/s-0028-1087130.

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Wilson, A. P., C. C. T. Smith, B. N. C. Prichard, and D. J. Betteridge. "Platelet catecholamines and platelet function in normal human subjects." Clinical Science 73, no. 1 (1987): 99–103. http://dx.doi.org/10.1042/cs0730099.

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1. We have used high-performance liquid chromatography with electrochemical detection to measure plasma and platelet catecholamines in 24 normal subjects. 2. In the same subjects platelet function was assessed by measuring platelet aggregation in response to adenosine 5′-pyrophosphate, thrombin, adrenaline and collagen. Platelet sensitivity to prostacyclin was also examined. 3. Platelet noradrenaline showed a positive correlation with extent of aggregation induced by ‘low-dose’ collagen (1 μg/ml). No correlation was seen at the higher collagen concentration. 4. Platelet noradrenaline content a

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Pignatelli, P., L. Lenti, V. Sanguigni, et al. "Carnitine inhibits arachidonic acid turnover, platelet function, and oxidative stress." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (2003): H41—H48. http://dx.doi.org/10.1152/ajpheart.00249.2002.

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Carnitine is a physiological cellular constituent that favors intracellular fatty acid transport, whose role on platelet function and O2free radicals has not been fully investigated. The aim of this study was to seek whether carnitine interferes with arachidonic acid metabolism and platelet function. Carnitine (10–50 μM) was able to dose dependently inhibit arachidonic acid incorporation into platelet phospholipids and agonist-induced arachidonic acid release. Incubation of platelets with carnitine dose dependently inhibited collagen-induced platelet aggregation, thromboxane A2formation, and C

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Ed Nignpense, Borkwei, Kenneth A. Chinkwo, Christopher L. Blanchard, and Abishek B. Santhakumar. "Polyphenols: Modulators of Platelet Function and Platelet Microparticle Generation?" International Journal of Molecular Sciences 21, no. 1 (2019): 146. http://dx.doi.org/10.3390/ijms21010146.

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Platelets and platelet microparticles (PMPs) play a key role in the pathophysiology of vascular disorders such as coronary artery disease and stroke. In atherosclerosis, for example, the disruption of the plaque exposes endogenous agonists such as collagen, which activates platelets. Platelet hyper-activation and the high levels of PMPs generated in such situations pose a thrombotic risk that can lead to strokes or myocardial infarctions. Interestingly, dietary polyphenols are gaining much attention due to their potential to mimic the antiplatelet activity of treatment drugs such as aspirin an

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Beaulieu, Lea, Kahraman Tanriverdi, Jane Freedman, and Lauren Clancy. "The role of RNA uptake in platelet heterogeneity." Thrombosis and Haemostasis 117, no. 05 (2017): 948–61. http://dx.doi.org/10.1160/th16-11-0873.

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SummaryThe role of platelets in regulating vascular homeostasis has expanded beyond mediation of haemostasis and thrombosis. The discovery of platelet RNA and the presence of subpopulations of platelets containing varying amounts of RNA suggest a role for platelet transcripts in vascular function. As the RNA in anucleated platelets is biologically functional and may transfer to other vascular cells, we hypothesised that platelet RNA diminishes over the lifespan of the platelet with diminishing platelet size due to horizontal cellular transfer. The purpose of this study is to determine if plate

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Nic an Riogh, Eithne, Eimear Dunne, Sharon Cowley, et al. "Dynamic platelet function: A novel biomarker in inflammatory arthritis?" PLOS ONE 17, no. 1 (2022): e0261825. http://dx.doi.org/10.1371/journal.pone.0261825.

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Background Patients with inflammatory arthritis die prematurely of cardiovascular disease. Inflammation activates platelets. Since treatment of inflammatory arthritis is associated with reduced mortality, and decreased platelet reactivity reduces cardiovascular events, we hypothesised that platelet reactivity as measured by dynamic platelet function (DPF) would be increased in patients with inflammatory arthritis and that reactivity could be reduced with therapeutic intervention. Objectives To characterise platelet function using a validated physiological assay in patients with inflammatory ar

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Maurer-Spurej, Elisabeth, and Kate Chipperfield. "Could Microparticles Be the Universal Quality Indicator for Platelet Viability and Function?" Journal of Blood Transfusion 2016 (December 8, 2016): 1–11. http://dx.doi.org/10.1155/2016/6140239.

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High quality means good fitness for the intended use. Research activity regarding quality measures for platelet transfusions has focused on platelet storage and platelet storage lesion. Thus, platelet quality is judged from the manufacturer’s point of view and regulated to ensure consistency and stability of the manufacturing process. Assuming that fresh product is always superior to aged product, maintaining in vitro characteristics should preserve high quality. However, despite the highest in vitro quality standards, platelets often fail in vivo. This suggests we may need different quality m

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Jacob, Shancy P., Yasuhiro Kosaka, Seema Bhatlekar, et al. "Mitofusin2 (MFN2) Preserves Mitochondrial Integrity and Function in Megakaryocytes and Platelets." Blood 138, Supplement 1 (2021): 3137. http://dx.doi.org/10.1182/blood-2021-154329.

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Abstract Genome wide association studies (GWAS) have associated mitochondria related loci with platelet numbers, function, and CVD. However, causality has not been established for many of these variants, and their mechanism and functional consequences are unknown. One such variant, MFN2 eQTL rs1474868 (T/T), has been associated with reduced platelet counts and reduced expression (5 fold) of MFN2 RNA in platelets. We show here that the MFN2 T/T variant corresponds with significantly reduced MFN2 protein in platelets. This difference contributes to a significant correlation between MFN2 RNA leve

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Peyvandi, Flora, Isabella Garagiola, Andrea Artoni, et al. "Localization and Function of Platelet ADAMTS-13." Blood 106, no. 11 (2005): 3967. http://dx.doi.org/10.1182/blood.v106.11.3967.3967.

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Abstract The haemostatic activity of von Willebrand factor (VWF) is strongly dependent on its multimeric size, with the highest activity in ‘unusually large’ multimers (ULVWF) secreted from endothelial cells. The multimeric size is regulated by a plasma metalloprotease, ADAMTS-13. Since 15–25% of circulating VWF is stored in platelets, the presence and function of ADAMTS-13 in platelets could be an important issue to be investigated. In our study, we showed the presence of ADAMTS-13 in human platelets consistently with observations reported by Suzuki M. et al (Biochem Biophys Res Commun, 2004)

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Rand, Margaret L., and Stefan Kuhle. "Platelets and platelet function testing in children." Progress in Pediatric Cardiology 21, no. 1 (2005): 63–69. http://dx.doi.org/10.1016/j.ppedcard.2005.09.008.

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Michelson, Alan D. "How Platelets Work: Platelet Function and Dysfunction." Journal of Thrombosis and Thrombolysis 16, no. 1/2 (2003): 7–12. http://dx.doi.org/10.1023/b:thro.0000014586.77684.82.

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Choi, Jae-Lim, Shuhua Li, and Jin-Yeong Han. "Platelet Function Tests: A Review of Progresses in Clinical Application." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/456569.

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The major goal of traditional platelet function tests has been to screen and diagnose patients who present with bleeding problems. However, as the central role of platelets implicated in the etiology of arterial thrombotic diseases such as myocardial infarction and stroke became widely known, platelet function tests are now being promoted to monitor the efficacy of antiplatelet drugs and also to potentially identify patients at increased risk of thrombosis. Beyond hemostasis and thrombosis, an increasing number of studies indicate that platelets play an integral role in intercellular communica

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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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Kral-Pointner, Julia Barbara, Waltraud Cornelia Schrottmaier, Manuel Salzmann, et al. "Platelet PI3K Modulates Innate Leukocyte Extravasation during Acid-Induced Acute Lung Inflammation." Thrombosis and Haemostasis 119, no. 10 (2019): 1642–54. http://dx.doi.org/10.1055/s-0039-1693693.

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Introduction Blood platelets are increasingly recognized as modulators of leukocyte effector functions in various pathologies including acute lung injury (ALI). ALI is a life-threatening disease, caused by damage to the alveolar epi- and endothelium. Excessive accumulation of leukocytes leads to severe lung inflammation, resulting in impaired lung function and hypoxemia. Objective Since leukocyte migration is modulated by activated platelets and phosphatidylinositol 3-kinase (PI3K) signaling is involved in platelet function, we aimed to elucidate the effect of PI3K on platelet-mediated immune

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Zou, Siying, Alexandra M. Teixeira, Chad D. Sanada, Ping-xia Zhang, and Diane Krause. "ARHGEF12 Is Essential for Human Megakaryocyte Differentiation and Plays Critical Roles in Platelet Function." Blood 124, no. 21 (2014): 341. http://dx.doi.org/10.1182/blood.v124.21.341.341.

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Abstract Megakaryocytopoiesis, the process by which hematopoietic stem cells develop into mature megakaryocytes (MK), and thrombopoiesis, platelet production/release, are critical for blood homeostasis. We tested the hypothesis that the Rho guanine exchange factor, ARHGEF12 (also known as LARG), is critical for MK differentiation and platelet functions based on the following: 1) ARHGEF12 is part of a recurrent translocation with MLL in acute myeloid leukemia. 2) Both published microarray datasets and deep-sequencing data from our lab on primary human CD34+ cells differentiating into MKs show t

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Kaneider, Nicole, Clemens Feistritzer, Donatella Gritti, et al. "Expression and function of syndecan-4 in human platelets." Thrombosis and Haemostasis 93, no. 06 (2005): 1120–27. http://dx.doi.org/10.1160/th04-11-0763.

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SummaryPlatelet recruitment crucially depends on amplification systems provided by autocrine and paracrine factors such as adenosine diphosphate. In inflammatory states, consumption of coagulation proteins, such as antithrombin aggravates the procoagulant state. In this study, we report that platelets express synde-can-4, an antithrombin-binding cell surface heparan sulphate proteoglycan, whose ligation with antithrombin inhibits activated platelet-dependent superoxide anion release from neut-rophils by the limitation of adenosine diphosphate and adeno-sine triphosphate secretion in activated

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Baldassarri, Samantha, Alessandra Bertoni, Paolo Lova, et al. "The Endocannabinoid 2-Arachidonoylglycerol Regulates Platelet Function." Blood 108, no. 11 (2006): 3904. http://dx.doi.org/10.1182/blood.v108.11.3904.3904.

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Abstract 2-Arachidonoylglycerol (2-AG) is a naturally occurring monoglyceride that activates cannabinoid receptors and meets several key requisites of an endogenous cannabinoid substance. It is present in the brain and hematopoietic cells, including macrophages, lymphocytes and platelets. 2-AG is released from cells in a stimulus-dependent manner and is rapidly eliminated by uptake into cells and enzymatic hydrolysis in arachidonic acid and glycerol. 2-AG might exert a very fine control on platelet function either through mechanisms intertwining with the signal transduction pathways used by pl

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Krause, Diane, Stephanie Halene, Carmen Jane Booth, et al. "Epithelial (E)-Cadherin Is a Novel Regulator of Platelet Function." Blood 124, no. 21 (2014): 95. http://dx.doi.org/10.1182/blood.v124.21.95.95.

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Abstract Epithelial (E-) cadherin is an adhesion molecule that mediates cell-cell interactions, and is important in pluripotent stem cell reprogramming. We are investigating the role of E-cadherin in megakaryocyte differentiation and platelet function, and propose that E-cadherin mediates interactions that facilitate the essential roles of platelets. We have evidence that mature megakaryocytes and platelets express E-cadherin, and therefore generated a megakaryocyte-specific E-cadherin knockout mouse using the PF4-Cre system. E-cadherin deleted mice are viable and fertile. Despite having norma

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El-Kadiry, Abed El-Hakim, and Yahye Merhi. "The Role of the Proteasome in Platelet Function." International Journal of Molecular Sciences 22, no. 8 (2021): 3999. http://dx.doi.org/10.3390/ijms22083999.

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Platelets are megakaryocyte-derived acellular fragments prepped to maintain primary hemostasis and thrombosis by preserving vascular integrity. Although they lack nuclei, platelets harbor functional genomic mediators that bolster platelet activity in a signal-specific manner by performing limited de novo protein synthesis. Furthermore, despite their limited protein synthesis, platelets are equipped with multiple protein degradation mechanisms, such as the proteasome. In nucleated cells, the functions of the proteasome are well established and primarily include proteostasis among a myriad of ot

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Tabuchi, Noriyuki, Izaak Tigchelaar, and Willem Van Oeveren. "Shear-Induced Pathway of Platelet Function in Cardiac Surgery." Seminars in Thrombosis and Hemostasis 21, S 02 (1995): 66–70. http://dx.doi.org/10.1055/s-0032-1313605.

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The contribution of platelet dysfunction to the impaired hemostasis after cardiac surgery remains to be established, because there is no sensitive method to assess platelet function. Measurement of the shear-induced pathway of platelet function, an important mechanism in inducing hemostasis, became possible by a novel shear-inducing technique, the in-vitro bleeding test (Thrombostat 4000). By using this test, the changes in platelet function during cardiopulmonary bypass and their contribution to hemostasis were investigated in patients undergoing cardiac surgery. Platelet function is quickly

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Ma, Liping, Da-Nian Nie, Xiu-Ju Wang, et al. "The Function of Toll-Like Receptor 4 Expressions on Human Platelet in Platelet Activation." Blood 112, no. 11 (2008): 5361. http://dx.doi.org/10.1182/blood.v112.11.5361.5361.

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Abstract Lipopolysaccsharide (LPS) is a principal outer membrane component of gram-negative bacteria. It initiates an inflammatory response to infection by activating Toll-like receptor-4 (TLR4) in host. Infection increases risk for hemostasis, thrombosis, DIC, and tissue repair. Platelet contributes to the inflammation process through respond to invading pathogens, membrane adhesion molecule (P-selectin) is one of the indexes to determine platelet activation. Experiment was designed to study whether TLR4 is expressed on human platelet, and what is the function of TLR4 in platelet activation i

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Ambrosio, G., P. Golino, I. Pascucci, et al. "Modulation of platelet function by reactive oxygen metabolites." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (1994): H308—H318. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h308.

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Reactive oxygen metabolites have been reported to affect platelet aggregation. However, this phenomenon is still poorly understood. In the present study we investigated the effects of superoxide radical and hydrogen peroxide (H2O2) on platelet function in vitro and correlated those effects to possible changes of platelet concentrations of cyclic nucleotides and thromboxane, since these systems play a key role in the response of platelets to activating stimuli. Human platelets were exposed to xanthine-xanthine oxidase (X-XO), a system that generates both superoxide radicals and H2O2. Sixty seco

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Psaila, Bethan, James B. Bussel, Matthew D. Linden, et al. "In Vivo Effects of Eltrombopag on Human Platelet Function." Blood 110, no. 11 (2007): 1301. http://dx.doi.org/10.1182/blood.v110.11.1301.1301.

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Abstract Eltrombopag, an orally-administered small-molecule agonist of the thrombopoietin receptor (c-Mpl), is under investigation as a treatment for immune thrombocytopenic purpura (ITP). Studies have indicated that eltrombopag does not ‘prime’ platelets for activation in vitro, and eltrombopag administration to healthy volunteers does not increase platelet surface P-selectin or activated integrin αIIbβ3 (Jenkins J. Blood 2007). However, the effects of eltrombopag on platelet function in thrombocytopenic patients in vivo, either by direct binding to c-Mpl receptors on platelets or indirectly

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Rigg, Rachel A., Laura D. Healy, Marie S. Nowak, et al. "Heat shock protein 70 regulates platelet integrin activation, granule secretion and aggregation." American Journal of Physiology-Cell Physiology 310, no. 7 (2016): C568—C575. http://dx.doi.org/10.1152/ajpcell.00362.2015.

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Molecular chaperones that support protein quality control, including heat shock protein 70 (Hsp70), participate in diverse aspects of cellular and physiological function. Recent studies have reported roles for specific chaperone activities in blood platelets in maintaining hemostasis; however, the functions of Hsp70 in platelet physiology remain uninvestigated. Here we characterize roles for Hsp70 activity in platelet activation and function. In vitro biochemical, microscopy, flow cytometry, and aggregometry assays of platelet function, as well as ex vivo analyses of platelet aggregate formati

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Gnatenko, Dmitri V., Peter L. Perrotta, and Wadie F. Bahou. "Proteomic approaches to dissect platelet function: half the story." Blood 108, no. 13 (2006): 3983–91. http://dx.doi.org/10.1182/blood-2006-06-026518.

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AbstractPlatelets play critical roles in diverse hemostatic and pathologic disorders and are broadly implicated in various biological processes that include inflammation, wound healing, and thrombosis. Recent progress in high-throughput mRNA and protein profiling techniques has advanced our understanding of the biological functions of platelets. Platelet proteomics has been adopted to decode the complex processes that underlie platelet function by identifying novel platelet-expressed proteins, dissecting mechanisms of signal or metabolic pathways, and analyzing functional changes of the platel

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