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Journal articles on the topic 'Human platelet'

Author: Grafiati

Published: 21 February 2023

Last updated: 25 July 2025

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1

POLGÁR, János, Ruth M. KRAMER, Suzane L. UM, Joseph A. JAKUBOWSKI, and Kenneth J. CLEMETSON. "Human group II 14 kDa phospholipase A2 activates human platelets." Biochemical Journal 327, no. 1 (1997): 259–65. http://dx.doi.org/10.1042/bj3270259.

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Recombinant human group II phospholipase A2 (sPLA2) added to human platelets in the low μg/ml range induced platelet activation, as demonstrated by measurement of platelet aggregation, thromboxane A2 generation and influx of intracellular free Ca2+ concentration and by detection of time-dependent tyrosine phosphorylation of platelet proteins. The presence of Ca2+ at low millimolar concentrations is a prerequisite for the activation of platelets by sPLA2. Mg2+ cannot replace Ca2+. Mg2+, given in addition to the necessary Ca2+, inhibits sPLA2-induced platelet activation. Pre-exposure to sPLA2 co

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2

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

Krisch, Linda, Gabriele Brachtl, Sarah Hochmann, et al. "Improving Human Induced Pluripotent Stem Cell-Derived Megakaryocyte Differentiation and Platelet Production." International Journal of Molecular Sciences 22, no. 15 (2021): 8224. http://dx.doi.org/10.3390/ijms22158224.

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Several protocols exist for generating megakaryocytes (MKs) and platelets from human induced pluripotent stem cells (hiPSCs) with limited efficiency. We observed previously that mesoderm induction improved endothelial and stromal differentiation. We, therefore, hypothesized that a protocol modification prior to hemogenic endothelial cell (HEC) differentiation will improve MK progenitor (MKP) production and increase platelet output. We further asked if basic media composition affects MK maturation. In an iterative process, we first compared two HEC induction protocols. We found significantly mo

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4

Kelm, RJ Jr, and KG Mann. "Human platelet osteonectin: release, surface expression, and partial characterization." Blood 75, no. 5 (1990): 1105–13. http://dx.doi.org/10.1182/blood.v75.5.1105.1105.

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Abstract Our laboratory has previously shown that osteonectin, an abundant noncollagenous bone protein, is contained in and secreted from human platelets. In this study, the distribution of osteonectin both in the supernatant and on the platelet surface after activation was measured by fluid-phase and solid-phase radioimmunoassay, respectively. Total cellular osteonectin was determined by RIA of guanidinium chloride extracted platelets and ranged from 0.65 to 2.2 micrograms/10(8) platelets or 135,000 to 457,000 molecules/platelet. Platelets treated with varying concentrations of collagen and t

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Kelm, RJ Jr, and KG Mann. "Human platelet osteonectin: release, surface expression, and partial characterization." Blood 75, no. 5 (1990): 1105–13. http://dx.doi.org/10.1182/blood.v75.5.1105.bloodjournal7551105.

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Our laboratory has previously shown that osteonectin, an abundant noncollagenous bone protein, is contained in and secreted from human platelets. In this study, the distribution of osteonectin both in the supernatant and on the platelet surface after activation was measured by fluid-phase and solid-phase radioimmunoassay, respectively. Total cellular osteonectin was determined by RIA of guanidinium chloride extracted platelets and ranged from 0.65 to 2.2 micrograms/10(8) platelets or 135,000 to 457,000 molecules/platelet. Platelets treated with varying concentrations of collagen and thrombin r

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6

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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7

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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8

Malmgren, R., T. Thorsen, R. T. Lie, and H. Holmsen. "Microbubble-Induced Serotonin Secretion in Human Platelets." Thrombosis and Haemostasis 65, no. 04 (1991): 399–402. http://dx.doi.org/10.1055/s-0038-1648160.

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SummaryThe effect of nitrogen (N2) microbubbles on platelets resembles that of common platelet agonists with respect to aggregation (Thorsen T et al., Undersea Biomed Res 1986; 13:289-303). In the present study we examined the effect of microbubbles on platelet secretion of preloaded 14C-serotonin. We demonstrate that stirring of platelet-rich plasma with N2-microbubbles causes a loss of single platelets that is associated with secretion. However, secretion did not increase above baseline values until after 20 min of microbubble exposure, when platelet aggregation had reached 40%. After that t

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9

Fong, Karen P., Colin Barry, Anh N. Tran, et al. "Deciphering the human platelet sheddome." Blood 117, no. 1 (2011): e15-e26. http://dx.doi.org/10.1182/blood-2010-05-283838.

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Abstract Activated platelets shed surface proteins, potentially modifying platelet function as well as providing a source of bioactive fragments. Previous studies have identified several constituents of the platelet sheddome, but the full extent of shedding is unknown. Here we have taken a global approach, analyzing protein fragments in the supernate of activated platelets using mass spectroscopy and looking for proteins originating from platelet membranes. After removing plasma proteins and microparticles, 1048 proteins were identified, including 69 membrane proteins. Nearly all of the membra

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10

Takahashi, Hoyu, and Akira Shibata. "Agglutination of Platelet-Type von Willebrand’s Disease Platelets by Bovine von Willebrand Factor." Thrombosis and Haemostasis 53, no. 02 (1985): 204–7. http://dx.doi.org/10.1055/s-0038-1661274.

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SummaryIt has been shown that platelets from patients with platelet- type von Willebrand’s disease (vWD) agglutinate upon the addition of human von Willebrand factor (vWF) in the absence of ristocetin or botrocetin, suggesting that platelet membrane receptors for human vWF is abnormal. The present work reports the platelet agglutinability on stimulation with bovine vWF in platelet-type vWD. Platelets in patient platelet-rich plasma or washed platelet suspensions and patient platelets treated with formalin agglutinated in the presence of markedly lower concentrations of bovine vWF than those re

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11

Kornecki, E., Y. H. Ehrlich, R. Egbring, et al. "Granulocyte-platelet interactions and platelet fibrinogen receptor exposure." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (1988): H651—H658. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h651.

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We have examined the interaction of human granulocyte elastase with human platelets. Incubation of human platelets with human granulocyte elastase exposed active fibrinogen-binding sites as evidenced by 125I-labeled fibrinogen binding and spontaneous fibrinogen-induced platelet aggregation. The aggregation of platelets by fibrinogen occurred at low concentrations of human granulocyte elastase (0.5–1 microgram/ml). Platelets pretreated with human granulocyte elastase exposed an average of 10,500 fibrinogen binding sites per platelet, i.e., about one-third the number of binding sites exposed by

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12

Heffner, J. E., S. A. Katz, P. V. Halushka, and J. A. Cook. "Human platelets attenuate oxidant injury in isolated rabbit lungs." Journal of Applied Physiology 65, no. 3 (1988): 1258–66. http://dx.doi.org/10.1152/jappl.1988.65.3.1258.

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Because platelets contain active antioxidant systems, the capacity of platelets to attenuate oxidant lung injury was investigated. Purine and xanthine oxidase were infused into isolated perfused rabbit lungs (IPL) to generate H2O2, thereby causing increased membrane permeability edema. The coinfusion of washed human platelets (1.20 +/- 0.07 x 10(10) cells) attenuated the degree of edema formation as measured by lung weight gain and lung lavage albumin concentration. Electron microscopy of lung preparations demonstrated platelet adherence to capillary endothelial luminal surfaces of oxidant-inj

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13

Schattner, M., M. Lazzari, AS Trevani, et al. "Activation of human platelets by immune complexes prepared with cationized human IgG." Blood 82, no. 10 (1993): 3045–51. http://dx.doi.org/10.1182/blood.v82.10.3045.3045.

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Abstract The present study shows that the ability of soluble immune complexes (IC), prepared with human IgG and rabbit IgG antibodies against human IgG, to trigger platelet activation was markedly higher for IC prepared with cationized human IgG (catIC) compared with those prepared with untreated human IgG (cIC). CatIC induced platelet aggregation and adenosine triphosphate release in washed platelets (WP), gel-filtered platelets (GFP), or platelet-rich plasma (PRP) at physiologic concentrations of platelets (3 x 10(8)/mL) and at low concentrations of catIC (1 to 30 micrograms/mL). On the cont

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14

Schattner, M., M. Lazzari, AS Trevani, et al. "Activation of human platelets by immune complexes prepared with cationized human IgG." Blood 82, no. 10 (1993): 3045–51. http://dx.doi.org/10.1182/blood.v82.10.3045.bloodjournal82103045.

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The present study shows that the ability of soluble immune complexes (IC), prepared with human IgG and rabbit IgG antibodies against human IgG, to trigger platelet activation was markedly higher for IC prepared with cationized human IgG (catIC) compared with those prepared with untreated human IgG (cIC). CatIC induced platelet aggregation and adenosine triphosphate release in washed platelets (WP), gel-filtered platelets (GFP), or platelet-rich plasma (PRP) at physiologic concentrations of platelets (3 x 10(8)/mL) and at low concentrations of catIC (1 to 30 micrograms/mL). On the contrary, und

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15

Liu, Xiao, Li Liu, Ana-Maria Zaske, et al. "Contact- and agonist-regulated microvesiculation of human platelets." Thrombosis and Haemostasis 110, no. 08 (2013): 331–99. http://dx.doi.org/10.1160/th12-11-0853.

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SummaryAfter exposure to an agonist, platelets are activated and become aggregated. They also shed membrane microparticles that participate in the pathogenesis of thrombosis, hyper-coagulation and inflammation. However, microvesiculation can potentially disrupt the integrity of platelet aggregation by shedding the membrane receptors and phosphatidylserine critical for forming and stabilising a platelet clot. We tested the hypothesis that adhesion and microvesiculation are functions of different subsets of platelets at the time of haemostasis by real-time monitoring of agonist-induced morpholog

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16

Mosnier, Laurent O., Paula Buijtenhuijs, Pauline F. Marx, Joost C. M. Meijers, and Bonno N. Bouma. "Identification of thrombin activatable fibrinolysis inhibitor (TAFI) in human platelets." Blood 101, no. 12 (2003): 4844–46. http://dx.doi.org/10.1182/blood-2002-09-2944.

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AbstractThrombin activatable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like proenzyme that after activation down-regulates fibrinolysis. Platelets are known to contain antifibrinolytic factors that are secreted during platelet activation. Therefore, the presence of TAFI in platelets was analyzed. TAFI was identified in platelets in a concentration of about 50 ng/1 × 109 platelets and was secreted on platelet activation. Thrombin-mediated activation of platelet-derived TAFI resembled that of plasma-derived TAFI with respect to stimulation by thrombomodulin and spontaneous loss of ac

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17

Kondkar, Altaf A., Wei Hong, Wolfgang Bergmeier, et al. "Transfection of Human Platelets Down-Regulates Endogenous mRNA." Blood 114, no. 22 (2009): 4026. http://dx.doi.org/10.1182/blood.v114.22.4026.4026.

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Abstract Abstract 4026 Poster Board III-962 Platelets are anucleate and, as such, lack the capacity for transcribing and expressing exogenously introduced genes or cDNAs. However, platelets contain megakaryocyte-transcribed mRNAs and respond to physiological stimuli by translating mRNA into protein. Compared to the megakaryocyte, the relative contribution of platelet translation to the platelet proteome is unknown. However, it is noteworthy that platelets in Blood Bank storage conditions increase their levels of integrin β3 over time and that the half-life of some mRNA is longer in platelets t

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18

Schwarz, HP, MJ Heeb, JD Wencel-Drake, and JH Griffin. "Identification and quantitation of protein S in human platelets." Blood 66, no. 6 (1985): 1452–55. http://dx.doi.org/10.1182/blood.v66.6.1452.bloodjournal6661452.

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Gel filtered human platelets contaminated with less than 0.02% of plasma protein S contained 490 ng of protein S antigen per 3 X 10(8) platelets, equivalent to 2.5% of protein S in whole blood. Three patients with heterozygous plasma protein S deficiency, a congenital disorder associated with venous thrombotic disease, had platelet protein S antigen levels that were 40% of the mean platelet level in ten normal volunteers. In immunoblotting analysis, platelet protein S was indistinguishable from plasma protein S. Thrombin stimulation of platelets caused release of 63% of total protein S antigen

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19

Sawicki, Grzegorz, Esmond Sanders, Eduardo Salas, Mieczyslaw Wozniak, Jose Rodrigo, and Marek Radomski. "Localization and Translocation of MMP-2 during Aggregation of Human Platelets." Thrombosis and Haemostasis 80, no. 11 (1998): 836–39. http://dx.doi.org/10.1055/s-0037-1615367.

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SummaryWe have previously shown that human platelets express matrix metalloproteinase-2 (MMP-2) and that the release of this enzyme during platelet activation mediates the ADP- and thromboxane-independent part of aggregation. We have now used immunogold electron microscopy, flow cytometry, Western blot analysis and zymography methods to study the ultrastructural localization of MMP-2 in human washed platelets. Platelet aggregation was stimulated by collagen and the MMP-2 immunoreactivity of platelets was followed during various stages of aggregation. In resting platelets, MMP-2 was randomly di

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20

Lijnen, H. R., B. Van Hoef, and D. Collen. "Interactions of Staphylokinase with Human Platelets." Thrombosis and Haemostasis 73, no. 03 (1995): 472–77. http://dx.doi.org/10.1055/s-0038-1653799.

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SummaryThe interactions of recombinant staphylokinase (SakSTAR) with human platelets were investigated in a buffer milieu, in a human plasma milieu in vitro, and in plasma from patients with acute myocardial infarction (AMI) treated with SakSTAR.In a buffer milieu, the activation rate of plasminogen by SakSTAR or streptokinase (SK) was not significantly altered by addition of platelets. Specific binding of SakSTAR or SK to either resting or thrombin- activated platelets was very low. ADP-induced or collagen-induced platelet aggregation in platelet-rich plasma (PRP) was 94 ± 2.7% or 101 ± 1.7%

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21

Schwarz, HP, MJ Heeb, JD Wencel-Drake, and JH Griffin. "Identification and quantitation of protein S in human platelets." Blood 66, no. 6 (1985): 1452–55. http://dx.doi.org/10.1182/blood.v66.6.1452.1452.

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Abstract Gel filtered human platelets contaminated with less than 0.02% of plasma protein S contained 490 ng of protein S antigen per 3 X 10(8) platelets, equivalent to 2.5% of protein S in whole blood. Three patients with heterozygous plasma protein S deficiency, a congenital disorder associated with venous thrombotic disease, had platelet protein S antigen levels that were 40% of the mean platelet level in ten normal volunteers. In immunoblotting analysis, platelet protein S was indistinguishable from plasma protein S. Thrombin stimulation of platelets caused release of 63% of total protein

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22

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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23

Cattaneo, M., B. Akkawat, R. L. Kinlough-Rathbone, M. A. Packham, C. Cimminiello, and P. M. Mannucci. "Ticlopidine Facilitates the Deaggregation of Human Platelets Aggregated by Thrombin." Thrombosis and Haemostasis 71, no. 01 (1994): 091–94. http://dx.doi.org/10.1055/s-0038-1642389.

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SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d

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24

Yong, E. C., E. Y. Chi, T. R. Fritsche, and W. R. Henderson. "Human platelet-mediated cytotoxicity against Toxoplasma gondii: role of thromboxane." Journal of Experimental Medicine 173, no. 1 (1991): 65–78. http://dx.doi.org/10.1084/jem.173.1.65.

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Human platelets, in the absence of antibody, are cytotoxic to tachyzoites of Toxoplasma gondii as determined by vital staining, transmission electron microscopy, and the failure of Toxoplasma to survive and replicate in mice after in vitro interaction of the organisms with platelets. Platelet to T. gondii ratios as low as 1:3 were toxic to the organisms with direct cell-cell contact essential for platelet-mediated cytotoxicity. Adherence of platelets to T. gondii and disruption of surface membranes and cytoplasmic contents of the organisms were observed ultrastructurally. Reactive oxygen speci

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25

Santos, Sascha Meyer dos, Kira Blankenbach, Klaus Scholich, et al. "Platelets from flowing blood attach to the inflammatory chemokine CXCL16 expressed in the endothelium of the human vessel wall." Thrombosis and Haemostasis 114, no. 08 (2015): 297–312. http://dx.doi.org/10.1160/th14-11-0911.

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SummaryEndothelial chemokine CXC motif ligand 16 (CXCL16) expression is associated with atherosclerosis, while platelets, particularly those attaching to atherosclerotic plaque, contribute to all stages of athero-sclerotic disease. This investigation was designed to examine the role of CXCL16 in capturing platelets from flowing blood. CXCL16 was expressed in human atherosclerotic plaques, and lesion severity in human carotid endarterectomy specimens was positively correlated with CXCL16 levels. CXCL16 expression in plaques was co-localised with platelets deposited to the endothelium. Immobilis

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Zhu, Wei, Wadie F. Bahou, and Dmitri V. Gnatenko. "Multiplexed genetic profiling of human blood platelets using fluorescent microspheres." Thrombosis and Haemostasis 100, no. 05 (2008): 929–36. http://dx.doi.org/10.1160/th08-05-0305.

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SummaryHuman platelets have unique and reproducible mRNA profiles, with evidence for distinct profiles in haematopoietic stem cell disorders associated with thrombocytosis. Platelet transcript profiling is traditionally studied by microarray analysis, quantitative reverse transcription-PCR or serial analysis of gene ex-pression,techniques that are labor- and technically-intensive.We have now applied a novel multiplex-based platform for quantitative transcript profiling of human platelets.Simultaneous quantification of 17 platelet transcripts was assayed using intact platelet-rich plasma or gel

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Pereira, Jaime, Kenji F. Shoji, Anibal A. Vargas, et al. "Human Platelets Express Functional Pannexin-1." Blood 118, no. 21 (2011): 1132. http://dx.doi.org/10.1182/blood.v118.21.1132.1132.

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Abstract Abstract 1132 The protein family of pannexins (Panx) contains three members (Panx1, Panx2 and Panx3) that are highly evolutionarily conserved from worms to mammals, and that form hemichannels involved in the transport of ions like Ca2+ and small molecules such as ATP into and out of cells. Panx1 is ubiquitously expressed in human tissues, and has been shown to mediate ATP release in erythrocytes, taste buds, airway epithelia and astrocytes. In platelets, ATP serves as an important paracrine and autocrine signaling molecule, binding to P2X1 purinergic receptors on the platelet surface,

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28

Uchiyama, Satoshi, Josh Sun, Kyoko Fukahori, et al. "Dual actions of group BStreptococcuscapsular sialic acid provide resistance to platelet-mediated antimicrobial killing." Proceedings of the National Academy of Sciences 116, no. 15 (2019): 7465–70. http://dx.doi.org/10.1073/pnas.1815572116.

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Circulating platelets have important functions in thrombosis and in modulating immune and inflammatory responses. However, the role of platelets in innate immunity to bacterial infection is largely unexplored. While human platelets rapidly killStaphylococcus aureus, we found the neonatal pathogen group BStreptococcus(GBS) to be remarkably resistant to platelet killing. GBS possesses a capsule polysaccharide (CPS) with terminal α2,3-linked sialic acid (Sia) residues that mimic a common epitope present on the human cell surface glycocalyx. A GBS mutant deficient in CPS Sia was more efficiently k

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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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Papa, Anne-Laure, Amanda Jiang, Netanel Korin, et al. "Platelet decoys inhibit thrombosis and prevent metastatic tumor formation in preclinical models." Science Translational Medicine 11, no. 479 (2019): eaau5898. http://dx.doi.org/10.1126/scitranslmed.aau5898.

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Platelets are crucial for normal hemostasis; however, their hyperactivation also contributes to many potentially lethal pathologies including myocardial infarction, stroke, and cancer. We hypothesized that modified platelets lacking their aggregation and activation capacity could act as reversible inhibitors of platelet activation cascades. Here, we describe the development of detergent-extracted human modified platelets (platelet decoys) that retained platelet binding functions but were incapable of functional activation and aggregation. Platelet decoys inhibited aggregation and adhesion of p

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Jennings, LK, RA Ashmun, WC Wang, and ME Dockter. "Analysis of human platelet glycoproteins IIb-IIIa and Glanzmann's thrombasthenia in whole blood by flow cytometry." Blood 68, no. 1 (1986): 173–79. http://dx.doi.org/10.1182/blood.v68.1.173.173.

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Abstract Antibodies that bind to human platelet membrane glycoproteins IIb and IIIa were used to develop methods for analyzing platelet membrane components by flow cytometry. Platelets were tentatively identified by their low-intensity light scatter profiles in whole blood or platelet- rich plasma preparations. Identification of this cell population as platelets was verified by using platelet-specific antibodies and fluorescein-conjugated antiimmunoglobulin. Two-parameter analysis of light scatter versus fluorescence intensity identified greater than 98% of the cells in the “platelet” light sc

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Jennings, LK, RA Ashmun, WC Wang, and ME Dockter. "Analysis of human platelet glycoproteins IIb-IIIa and Glanzmann's thrombasthenia in whole blood by flow cytometry." Blood 68, no. 1 (1986): 173–79. http://dx.doi.org/10.1182/blood.v68.1.173.bloodjournal681173.

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Antibodies that bind to human platelet membrane glycoproteins IIb and IIIa were used to develop methods for analyzing platelet membrane components by flow cytometry. Platelets were tentatively identified by their low-intensity light scatter profiles in whole blood or platelet- rich plasma preparations. Identification of this cell population as platelets was verified by using platelet-specific antibodies and fluorescein-conjugated antiimmunoglobulin. Two-parameter analysis of light scatter versus fluorescence intensity identified greater than 98% of the cells in the “platelet” light scatter pro

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Sottile, Jane, Deane F. Mosher, Jan Fullenweider, and James N. George. "Human Platelets Contain mRNA Transcripts for Platelet Factor 4 and Actin." Thrombosis and Haemostasis 62, no. 04 (1989): 1100–1102. http://dx.doi.org/10.1055/s-0038-1647125.

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SummaryRNAs from a number of cells, including platelets, were analyzed by Northern blotting for the presence of transcripts to four platelet proteins - actin, thrombospondin, fibronectin, and platelet factor 4. RNA from platelets contains considerable amounts of mRNA for platelet factor 4, easily detectable mRNA for actin, and traces of mRNA for thrombospondin. mRNA for platelet factor 4 was not detected in human lymphocytes or in any of 5 human cell lines.

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Szymańska, Patrycja, Bogusława Luzak, Katarzyna Miłowska, and Jacek Golański. "The Anti-Aggregative Potential of Resolvin E1 on Human Platelets." Molecules 28, no. 14 (2023): 5323. http://dx.doi.org/10.3390/molecules28145323.

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Resolvin E1 is a metabolite of eicosapentaenoic acid (EPA) which is one of the omega-3 polyunsaturated fatty acids (omega-3 PUFAs). The antiplatelet properties of omega-3 PUFAs are well known, but the effect of resolvin E1 on platelets via the collagen receptors is extremely poorly reported. We investigated the effect of resolvin E1 on collagen-induced platelet aggregation, activation, and reactivity, and also platelet membrane fluidity. The ultimate and statistically significant results showed that resolvin E1 may inhibit platelet reactivity due to the reduction of collagen-induced platelet a

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35

Burgers, JA, RC Schweizer, L. Koenderman, PL Bruijnzeel, and JW Akkerman. "Human platelets secrete chemotactic activity for eosinophils." Blood 81, no. 1 (1993): 49–55. http://dx.doi.org/10.1182/blood.v81.1.49.49.

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Abstract Thrombin-stimulated platelets liberate factors that induce chemotaxis of eosinophils and raise their cytosolic Ca2+ content ([Ca2+]i). The sources of this activity are the dense- and alpha-granules because inhibition of prostaglandin endoperoxide/thromboxane A2 formation and the platelet-activating factor receptor-antagonist WEB 2086 have no effect. Platelets from patients with Storage-Pool Deficiency show about 60% of the normal chemotactic activity with little effect on [Ca2+]i, whereas completely degranulated platelets fail to affect eosinophils. In concentrations secreted by the p

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Burgers, JA, RC Schweizer, L. Koenderman, PL Bruijnzeel, and JW Akkerman. "Human platelets secrete chemotactic activity for eosinophils." Blood 81, no. 1 (1993): 49–55. http://dx.doi.org/10.1182/blood.v81.1.49.bloodjournal81149.

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Thrombin-stimulated platelets liberate factors that induce chemotaxis of eosinophils and raise their cytosolic Ca2+ content ([Ca2+]i). The sources of this activity are the dense- and alpha-granules because inhibition of prostaglandin endoperoxide/thromboxane A2 formation and the platelet-activating factor receptor-antagonist WEB 2086 have no effect. Platelets from patients with Storage-Pool Deficiency show about 60% of the normal chemotactic activity with little effect on [Ca2+]i, whereas completely degranulated platelets fail to affect eosinophils. In concentrations secreted by the platelets,

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Zamora, C. A., D. Baron, and J. E. Heffner. "Washed human platelets prevent ischemia-reperfusion edema in isolated rabbit lungs." Journal of Applied Physiology 70, no. 3 (1991): 1075–84. http://dx.doi.org/10.1152/jappl.1991.70.3.1075.

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Washed human platelets prevent edema formation in isolated rabbit lungs infused with xanthine oxidase, an enzyme that injures endothelial membranes by generating extracellular oxidants. We hypothesized that platelets would similarly preserve membrane permeability in isolated lungs exposed to ischemia-reperfusion injury, a model that perturbs endothelial cells by the generation of intracellular oxidants. Isolated perfused rabbit lungs (IPL) were exposed to warm ischemia-reperfusion to cause lung edema. The infusion of washed human platelets (1.05 +/- 0.02 x 10(10) cells) prevented edema formati

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Tunjungputri, Rahajeng N., Esther Peters, Andre van der Ven, Philip G. de Groot, Quirijn de Mast, and Peter Pickkers. "Human recombinant alkaline phosphatase inhibits ex vivo platelet activation in humans." Thrombosis and Haemostasis 116, no. 12 (2016): 1111–21. http://dx.doi.org/10.1160/th16-03-0206.

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SummarySepsis-associated acute kidney injury (AKI) is associated with high morbidity and mortality. Excessive platelet activation contributes to AKI through the formation of microthrombi and amplification of systemic inflammation. Two phase II trials demonstrated that bovine-intestinal alkaline phosphatase (AP) improved renal function in critically ill patients with sepsis-associated AKI. In this study, we characterised the platelet-inhibiting effects of a human recombinant AP. Whole blood and platelet-rich plasma (PRP) of healthy volunteers (n=6) was pre-treated ex vivo with recAP, whereafter

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39

Kawasaki, T., Y. Taniuchi, N. Hisamichi, et al. "Tokaracetin, a new platelet antagonist that binds to platelet glycoprotein ib and inhibits von Willebrand factor-dependent shear-induced platelet aggregation." Biochemical Journal 308, no. 3 (1995): 947–53. http://dx.doi.org/10.1042/bj3080947.

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A new platelet antagonist, tokaracetin, was isolated from the venom of Trimeresurus tokarensis by ion-exchange chromatography, heparin-Sepharose chromatography and hydrophobic HPLC. The purified protein showed an apparent molecular mass on SDS/PAGE of 28.9 kDa under non-reducing conditions. On reduction, 16.1 and 15.4 kDa subunits were observed, suggesting that the molecule is a heterodimer. Tokaracetin inhibited the binding of 125I-labelled bovine von Willebrand factor (vWF) and 125I-labelled human vWF in the presence of botrocetin to fixed human platelets. It did not block ADP-, collagen- or

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40

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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Kruithof, E. K. O., C. Tran-Thang, and F. Bachmann. "Studies on the Release of a Plasminogen Activator Inhibitor by Human Platelets." Thrombosis and Haemostasis 55, no. 02 (1986): 201–5. http://dx.doi.org/10.1055/s-0038-1661522.

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SummaryThe relative contribution of platelets to plasminogen activator inhibitor (PA-inhibitor) activity in blood was investigated. From the difference in PA-inhibitor levels in platelet-poor plasmas of 12 donors (3 ± 1 U/ml, mean ±95% confidence limits) and in the corresponding platelet-rich plasmas after induction of platelet aggregation by collagen, ADP or epinephrine (7 ± 1 U/ml), it may be concluded that a greater amount of PA-inhibitor in blood is associated with platelets than with plasma. In collagen-stimulated platelets maximal release of PA-inhibitor and of beta-thromboglobulin (β-TG

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Sáez, Claudia G., Valeria Matus, Olga Panes, Jaime Pereira та Diego Mezzano. "Human Platelets Express and Synthesize CD3-ε Chain". Blood 112, № 11 (2008): 5363. http://dx.doi.org/10.1182/blood.v112.11.5363.5363.

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Abstract The function of platelets in hemostasis is well known, but only recently their role in modulating the adaptive immune response has been increasingly recognized. Platelets are able to stimulate B lymphocytes, enhance T lymphocytes responses and to adhere to dendritic cells modulating their activation. In addition to their ability to release a wide variety of inflammatory mediators, activated platelets can directly interact with pathogens, releasing attractant mediators for immune cells and acting as antigen presenting cells themselves. Once activated, platelets express numerous immune

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43

Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.382.

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Abstract A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich p

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44

Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.bloodjournal652382.

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A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and

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45

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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Peerschke, E. I., and B. Ghebrehiwet. "Human blood platelets possess specific binding sites for C1q." Journal of Immunology 138, no. 5 (1987): 1537–41. http://dx.doi.org/10.4049/jimmunol.138.5.1537.

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Abstract Although platelet interactions with C1q are implied by the inhibitory effect of C1q on collagen-induced platelet aggregation, specific receptors have not as yet been identified. To address the question of platelet receptors for free C1q, direct radioligand binding studies were performed by using human blood platelets and purified, 125I-labeled C1q, and a monoclonal antibody (II1/D1) (IgM, lambda) directed against C1q receptors on peripheral blood leukocytes. Washed platelets bound both purified 125I-labeled C1q and II1/D1 in a specific and saturable manner under physiologic ionic stre

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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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Cooling, Laura L. W., Kathleen Kelly, James Barton, Debbie Hwang, Theodore A. W. Koerner, and John D. Olson. "Determinants of ABH expression on human blood platelets." Blood 105, no. 8 (2005): 3356–64. http://dx.doi.org/10.1182/blood-2004-08-3080.

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AbstractPlatelets express ABH antigens, which can adversely effect platelet transfusion recovery and survival in ABH-incompatible recipients. To date, there has been no large, comprehensive study comparing specific donor factors with ABH expression on platelet membranes and glycoconjugates. We studied ABH expression in 166 group A apheresis platelet donors by flow cytometry, Western blotting, and thin layer chromatography relative to donor age, sex, A1/A2 subgroup, and Lewis phenotype. Overall, A antigen on platelet membranes, glycoproteins, and glycosphingolipids was linked to an A1 red blood

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49

Leytin, Valery, David J. Allen, Sergiy Mykhaylov, Elena Lyubimov, and John Freedman. "Thrombin Is Able To Trigger Apoptosis of Human Platelets." Blood 108, no. 11 (2006): 1094. http://dx.doi.org/10.1182/blood.v108.11.1094.1094.

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Abstract Although primarily known as a coagulation factor and as an inducer of platelet activation and aggregation, thrombin can modulate apoptosis in nucleated cells. Over the last decade, it has been recognized that apoptosis occurs not only in nucleated cells but also in anucleated cytoplasts and platelets. The current study investigated whether thrombin can impact apoptosis in anucleated human platelets. Using flow cytometry, we studied platelet apoptosis at the single cell level, analyzing markers of mitochondrial and cytoplasmic apoptosis (Leytin et al, Biochem Biophys Res Commun320:303,

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Parbtani, Anwar, William F. Clark, Anita Caveney, and Bruce Reid. "Binding of Aggregated Immunoglobulins to the Human Platelet Fc Receptors: A Mechanism of Platelet to Platelet Bridging." Thrombosis and Haemostasis 58, no. 04 (1987): 966–70. http://dx.doi.org/10.1055/s-0038-1646038.

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SummaryAggregated immunoglobulins react with human platelets by occupying the Fc receptors present on their surface, inducing aggregation and the release reaction. We studied the effect of heat aggregated gammaglobulins (HAGG) on ADP-induced aggregation of platelets. We used the minimum concentration of ADP required to induce a reversible aggregation of platelets without any substantial amount of serotonin (14C 5HT) release. EDTA (5 mM) added at the peak of platelet aggregation resulted in rapid deaggrcgation ot these platelets. However, incubation of platelets with HAGG at a dose that did not

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