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Journal articles on the topic 'Platelet response'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

DeHelian, Daniel, Shuchi Gupta, Jie Wu, et al. "RGS10 and RGS18 differentially limit platelet activation, promote platelet production, and prolong platelet survival." Blood 136, no. 15 (2020): 1773–82. http://dx.doi.org/10.1182/blood.2019003251.

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Abstract G protein–coupled receptors are critical mediators of platelet activation whose signaling can be modulated by members of the regulator of G protein signaling (RGS) family. The 2 most abundant RGS proteins in human and mouse platelets are RGS10 and RGS18. While each has been studied individually, critical questions remain about the overall impact of this mode of regulation in platelets. Here, we report that mice missing both proteins show reduced platelet survival and a 40% decrease in platelet count that can be partially reversed with aspirin and a P2Y12 antagonist. Their platelets ha

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2

Kim, Soochong, and Satya P. Kunapuli. "Negative Regulation of Gq-Mediated Pathways in Platelets by G12/13 Pathways through Fyn Kinase." Blood 112, no. 11 (2008): 2854. http://dx.doi.org/10.1182/blood.v112.11.2854.2854.

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Abstract Platelets contain high levels of Src family kinases (SFKs) suggesting an important role for these enzymes in platelet function. In this study, we have investigated the regulation of platelet function by SFKs downstream of G12/13 pathways. Calcium-independent platelet shape change induced by selective G12/13 stimulation with YFLLRNP was potentiated with a small mobilization of intracellular calcium in the presence of SFK inhibitors PP1 or PP2, which was abolished by the chelation of intracellular calcium, suggesting that SFKs downstream of G12/13 negatively regulate calcium mobilizatio

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3

Naylor-Adamson, Leigh, Zoe Booth, Simon Hart та ін. "Bruton's Tyrosine Kinase Inhibitors Impair Fcγriia-Mediated Responses of Healthy Donor Platelets and Chronic Lymphocytic Leukaemia Derived Platelets to Bacteria". Blood 136, Supplement 1 (2020): 1. http://dx.doi.org/10.1182/blood-2020-142624.

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Platelets play a key role in innate immunity and can interact with bacteria through multiple molecular mechanisms. One key receptor for platelet-bacteria interactions is FcγRIIa, a low affinity IgG immune receptor found on the surface of platelets, which is associated with platelet aggregation, phagocytosis and the release of bactericidal substances and cytokines from alpha and dense granules. The signalling pathways that regulate FcγRIIa mediated platelet responses to bacteria are not fully understood. Downstream of the FcγRIIa receptor is the protein Bruton's tyrosine kinase (Btk) and potent

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4

Auger, Jocelyn, Imke Munnix, Judith Cosemans, and Johan Heemskerk. "Platelet response heterogeneity in thrombus formation." Thrombosis and Haemostasis 102, no. 12 (2009): 1149–56. http://dx.doi.org/10.1160/th09-05-0289.

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SummaryVascular injury leads to formation of a structured thrombus as a consequence of platelet activation and aggregation, thrombin and fibrin formation, and trapping of leukocytes and red cells. This review summarises current evidence for heterogeneity of platelet responses and functions in the thrombus-forming process. Environmental factors contribute to response heterogeneity, as the platelets in a thrombus adhere to different substrates, and sense specific (ant)agonists and rheological conditions. Contraction of platelets and interaction with fibrin and other blood cells cause further res

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5

Norol, Françoise, Philippe Bierling, Françoise Roudot-Thoraval, et al. "Platelet Transfusion: A Dose-Response Study." Blood 92, no. 4 (1998): 1448–53. http://dx.doi.org/10.1182/blood.v92.4.1448.

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Abstract Early recommendations on prophylactic transfusion of thrombocytopenic patients involved a standard platelet dose of about 0.5 × 1011/10 kg body weight. Given the lack of data supporting this dose, we prospectively studied the dose response to platelet transfusions in adults and children with hematologic malignancies. Each patient received, in similar clinical conditions, a medium, high, and very high dose of fresh (&lt; 24 hours old) ABO-compatible platelets, in the form of apheresis platelet concentrates (APC). For the adults, the medium dose was defined as APC containing between

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6

Norol, Françoise, Philippe Bierling, Françoise Roudot-Thoraval, et al. "Platelet Transfusion: A Dose-Response Study." Blood 92, no. 4 (1998): 1448–53. http://dx.doi.org/10.1182/blood.v92.4.1448.416k10_1448_1453.

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Early recommendations on prophylactic transfusion of thrombocytopenic patients involved a standard platelet dose of about 0.5 × 1011/10 kg body weight. Given the lack of data supporting this dose, we prospectively studied the dose response to platelet transfusions in adults and children with hematologic malignancies. Each patient received, in similar clinical conditions, a medium, high, and very high dose of fresh (< 24 hours old) ABO-compatible platelets, in the form of apheresis platelet concentrates (APC). For the adults, the medium dose was defined as APC containing between 4 and 6 × 10

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7

Chouchane, Osoul, Valentine Léopold, Christine C. A. van Linge, et al. "Role of Liver Kinase 1B in Platelet Activation and Host Defense During Klebsiella pneumoniae-Induced Pneumosepsis." International Journal of Molecular Sciences 26, no. 8 (2025): 3714. https://doi.org/10.3390/ijms26083714.

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Pneumonia is the most common cause of sepsis, with Klebsiella pneumoniae frequently implicated as a causative pathogen. Platelets play a crucial role in host defense during sepsis, and their activation is essential for effective immune responses, which is at least in part induced through activation of the collagen receptor glycoprotein (GP)VI. Platelets require energy for their activation, and Liver kinase B1 (LKB1) is a key regulator of energy metabolism. We sought to determine the role of LKB1 in platelet function and host response during K. pneumoniae-induced pneumosepsis. Platelet-specific

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8

Cloutier, Nathalie, Isabelle Allaeys, Genevieve Marcoux, et al. "Platelets release pathogenic serotonin and return to circulation after immune complex-mediated sequestration." Proceedings of the National Academy of Sciences 115, no. 7 (2018): E1550—E1559. http://dx.doi.org/10.1073/pnas.1720553115.

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There is a growing appreciation for the contribution of platelets to immunity; however, our knowledge mostly relies on platelet functions associated with vascular injury and the prevention of bleeding. Circulating immune complexes (ICs) contribute to both chronic and acute inflammation in a multitude of clinical conditions. Herein, we scrutinized platelet responses to systemic ICs in the absence of tissue and endothelial wall injury. Platelet activation by circulating ICs through a mechanism requiring expression of platelet Fcγ receptor IIA resulted in the induction of systemic shock. IC-drive

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9

Page, Martin J., and Etheresia Pretorius. "A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection." Seminars in Thrombosis and Hemostasis 46, no. 03 (2020): 302–19. http://dx.doi.org/10.1055/s-0040-1708827.

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AbstractThrombocytopenia is commonly associated with sepsis and infections, which in turn are characterized by a profound immune reaction to the invading pathogen. Platelets are one of the cellular entities that exert considerable immune, antibacterial, and antiviral actions, and are therefore active participants in the host response. Platelets are sensitive to surrounding inflammatory stimuli and contribute to the immune response by multiple mechanisms, including endowing the endothelium with a proinflammatory phenotype, enhancing and amplifying leukocyte recruitment and inflammation, promoti

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10

Stalker, Timothy J. "Platelet Activation Gradients During Thrombus Formation." Blood 126, no. 23 (2015): SCI—13—SCI—13. http://dx.doi.org/10.1182/blood.v126.23.sci-13.sci-13.

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The hemostatic response requires the tightly regulated interaction of the coagulation system, platelets, other blood cells and components of the vessel wall at a site of vascular injury. The dysregulation of this response may result in excessive bleeding if the response is impaired, and pathologic thrombosis with vessel occlusion and tissue ischemia if the response is overly robust. Extensive studies over the past decades have sought to unravel the regulatory mechanisms that coordinate the multiple biochemical and cellular responses in time and space to ensure that an optimal response to vascu

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11

Haley, Kristina M., Cassandra P. Loren, Kevin G. Phillips, and Owen J. T. McCarty. "Characterization of Single Platelet Mass, Volume, and Density in Response to Agonist Stimulation." Blood 118, no. 21 (2011): 5261. http://dx.doi.org/10.1182/blood.v118.21.5261.5261.

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Abstract Abstract 5261 An increase in mean platelet volume (MPV) is correlated with platelet activation and subsequent shape change. Pathologic processes marked by increased platelet activity such as myocardial infarction, cerebral vascular accidents, diabetes mellitus, and hypertension are associated with an increased MPV. Elevated MPV in these conditions reflect both a higher level of platelet activation as well as increased platelet turnover secondary to platelet consumption within thrombus formation. Assessment of MPV can be used to risk stratify patients as well as assign them to prognost

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12

Setarehaseman, Alireza, Abbas Mohammadi, and Robert W. Maitta. "Thrombocytopenia in Sepsis." Life 15, no. 2 (2025): 274. https://doi.org/10.3390/life15020274.

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Platelets, traditionally known for their role in hemostasis, have emerged as key players in immune response and inflammation. Sepsis, a life-threatening condition characterized by systemic inflammation, often presents with thrombocytopenia, which at times, can be significant. Platelets contribute to the inflammatory response by interacting with leukocytes, endothelial cells, and the innate immune system. However, excessive platelet activation and consumption can lead to thrombocytopenia and exacerbate the severity of sepsis. Understanding the multifaceted roles of platelets in sepsis is crucia

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13

Li, Chen, Preeti Maurya, Benjamin Nieves-Lopez, Sara Ture, and Craig N. Morrell. "Platelet Mediated Monocyte/Macrophage Immune Training." Blood 138, Supplement 1 (2021): 3127. http://dx.doi.org/10.1182/blood-2021-151243.

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Abstract Platelets are essential mediators of vascular and immune homeostasis as well as mediators of thrombosis. Platelet functions in hemostasis and thrombosis have received great attention in both basic and clinical research, however, emerging research indicates platelets are also critical components of the immune system. Platelets have important roles in many inflammation-associated diseases including sepsis, atherosclerosis, and peripheral artery disease. In recent years, much interest has focused on the acute outcomes of interactions between platelets and monocytes/macrophages in immune

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14

Jones, C. R., R. McCabe, C. A. Hamilton, and J. L. Reid. "Maternal and Fetal Platelet Responses and Adrenoceptor Binding Characteristics." Thrombosis and Haemostasis 53, no. 01 (1985): 095–98. http://dx.doi.org/10.1055/s-0038-1661244.

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SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to th

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15

Chen, Xi, Shuchi Gupta, Matthew Cooper, et al. "GRK6 Regulates the Hemostatic Response to Injury through Its Rate-Limiting Effects on GPCR Signaling in Platelets." Blood 134, Supplement_1 (2019): 3611. http://dx.doi.org/10.1182/blood-2019-129175.

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Inappropriate platelet activation remains a major cause of cardiovascular and cerebrovascular diseases. Most agonists activate platelets through G protein-coupled receptors (GPCRs). However, questions remain about mechanisms that provide negative feedback towards activated GPCRs to limit platelet activation and thrombus formation. Here we provide the first evidence that GPCR kinase 6 (GRK6) serves this role in platelets, using GRK6-/- mice generated by CRISPR-Cas9 genome editing to examine the consequences of GRK6 knockout on GPCR-dependent signaling. Hemostatic thrombi formed in GRK6-/- mice

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16

O'Malley, CJ, JE Rasko, RL Basser, et al. "Administration of pegylated recombinant human megakaryocyte growth and development factor to humans stimulates the production of functional platelets that show no evidence of in vivo activation." Blood 88, no. 9 (1996): 3288–98. http://dx.doi.org/10.1182/blood.v88.9.3288.bloodjournal8893288.

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This report describes the effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on platelet production and platelet function in humans. Subjects with advanced solid tumors received PEG-rHuMGDF daily for up to 10 days. There was no increase in circulating platelet count at doses of 0.03 or 0.1 microgram/kg/d by day 12 of study. At doses of 0.3 and 1.0 microgram/kg/d there was a threefold median increase (maximum 10-fold) in platelet count by day 16. The platelets produced in vivo in response to PEG-rHuMGDF showed unchanged aggregation and adenosine trip

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17

Awamura, Thomas, Elizabeth S. Nakasone, Louie Mar Gangcuangco, et al. "Platelet and HIV Interactions and Their Contribution to Non-AIDS Comorbidities." Biomolecules 13, no. 11 (2023): 1608. http://dx.doi.org/10.3390/biom13111608.

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Platelets are anucleate cytoplasmic cell fragments that circulate in the blood, where they are involved in regulating hemostasis. Beyond their normal physiologic role, platelets have emerged as versatile effectors of immune response. During an infection, cell surface receptors enable platelets to recognize viruses, resulting in their activation. Activated platelets release biologically active molecules that further trigger host immune responses to protect the body against infection. Their impact on the immune response is also associated with the recruitment of circulating leukocytes to the sit

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18

Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.bloodjournal6761568.

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A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule secretion w

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19

Packham, M. A., N. L. Bryant, M. A. Guccione, R. L. Kinlough-Rathbone, and J. F. Mustard. "Effect of the Concentration of Ca2+ in the Suspending Medium on the Responses of Human and Rabbit Platelets to Aggregating Agents." Thrombosis and Haemostasis 62, no. 03 (1989): 968–76. http://dx.doi.org/10.1055/s-0038-1651037.

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SummaryThe effect of the concentration of Ca2+ in the suspending medium of human and rabbit platelets on aggregation, release of 14C-serotonin, and TXB2 formation in response to ADP, thrombin, l-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (PAF), collagen and arachidonic acid was studied in either platelet-rich plasma anticoagulated with D-phenylalanyl-prolyl-arginyl chloromethylketone (PPACK) or citrate, or suspensions of washed platelets in modified Tyrode-albumin solutions containing 1 mM Mg2+ and concentrations of added Ca2+ ranging from 0 to 5 mM. In response to ADP, thrombin, or PAF,

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20

Lopez, J. A., M. L. Armstrong, A. F. Brotherton, D. J. Piegors, and D. D. Heistad. "Effects of atherosclerosis and regression on vascular responses to products of activated platelets in primates." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (1991): H1051—H1056. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1051.

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We aggregated human platelets in vitro and examined vascular responses to injection of the supernatant in atherosclerotic primates. Platelets were washed, suspended, and aggregated with thrombin. Thrombin was then inactivated with D-Phe-Pro-ArgCH2Cl, and the suspension was centrifuged. The supernatant was injected intra-arterially into the perfused hindlimb within 30 s after aggregation of platelets. We studied normal cynomolgus monkeys, atherosclerotic monkeys that were fed atherogenic diet for 18 mo, and regression monkeys that were fed an atherogenic diet for 18 mo followed by a normal diet

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21

Peerschke, E. I., and B. Ghebrehiwet. "C1q augments platelet activation in response to aggregated Ig." Journal of Immunology 159, no. 11 (1997): 5594–98. http://dx.doi.org/10.4049/jimmunol.159.11.5594.

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Abstract Immune complexes and aggregated IgG (agg-IgG) induce platelet aggregation and the release reaction. Immune complexes also activate the complement system and interact with the complement component C1q. Since platelets possess both Fc and C1q receptors capable of signal transduction, the present study focused on the interaction between these binding sites and platelet activation. Subaggregating doses of agg-IgG (20-400 microg/ml) were identified for washed platelets from each of 11 healthy donors, and platelet aggregation was monitored in the presence or the absence of increasing concen

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22

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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23

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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24

Rahman, Mohammad Mizanur, Lutfunnahar Khan, and Debashish Saha. "Dose- and time-related platelet response with apheresis platelet concentrates and pooled platelets." Bangabandhu Sheikh Mujib Medical University Journal 10, no. 1 (2017): 44. http://dx.doi.org/10.3329/bsmmuj.v10i1.31667.

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<p>This present study was carried out to compare the post-transfusion platelet increment between the apheresis platelet concentrate (n=74) and pooled platelets (n=54). Pre- and post-transfusion platelet count of the recipient were carried out by automated hematology analyzer. In apheresis platelet concentrate group, the mean 24 hours post-transfusion platelet increment was 47 x 10<sup>9</sup>/L which was statistically significant (p&lt;0.001). On the other hand, in pooled platelets group, the mean 24 hours post–transfusions platelet count increment was 11.0 x 10<sup&gt

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25

Nührenberg, Thomas, Michael Amann, Marco Cederqvist, et al. "Impact of reticulated platelets on antiplatelet response to thienopyridines is independent of platelet turnover." Thrombosis and Haemostasis 116, no. 11 (2016): 941–48. http://dx.doi.org/10.1160/th16-03-0191.

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SummaryReticulated platelets are associated with impaired antiplatelet response to thienopyridines. It is uncertain whether this interaction is caused by a decreased drug exposure due to high platelet turnover reflected by elevated levels of reticulated platelets or by intrinsic properties of reticulated platelets. This study sought to investigate if the impact of reticulated platelets on early antiplatelet response to thienopyridines is mainly caused by platelet turnover as previously suggested. Elective patients undergoing coronary intervention were randomised to loading with clopidogrel 600

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26

Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.1568.

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Abstract A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule se

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27

Moog, Sylvie, Pierre Mangin, Nadège Lenain, et al. "Platelet glycoprotein V binds to collagen and participates in platelet adhesion and aggregation." Blood 98, no. 4 (2001): 1038–46. http://dx.doi.org/10.1182/blood.v98.4.1038.

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Glycoprotein V (GPV) is a subunit of the platelet GPIb-V-IX receptor for von Willebrand factor and thrombin. GPV is cleaved from the platelet surface during activation by thrombin, but its role in hemostasis is still unknown. It is reported that GPV knockout mice had a decreased tendency to form arterial occluding thrombi in an intravital thrombosis model and abnormal platelet interaction with the subendothelium. In vitro, GPV-deficient platelets exhibited defective adhesion to a collagen type I–coated surface under flow or static conditions. Aggregation studies demonstrated a decreased respon

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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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29

Theilmeier, Gregor, Carine Michiels, Erik Spaepen, et al. "Endothelial von Willebrand factor recruits platelets to atherosclerosis-prone sites in response to hypercholesterolemia." Blood 99, no. 12 (2002): 4486–93. http://dx.doi.org/10.1182/blood.v99.12.4486.

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Platelets are thought to play a causal role during atherogenesis. Platelet-endothelial interactions in vivo and their molecular mechanisms under shear are, however, incompletely characterized. Here, an in vivo platelet homing assay was used in hypercholesterolemic rabbits to track platelet adhesion to plaque predilection sites. The role of platelet versus aortic endothelial cell (EC) activation was studied in an ex vivo flow chamber. Pathways of human platelet immobilization were detailed during in vitro perfusion studies. In rabbits, a 0.125% cholesterol diet induced no lesions within 3 month

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Jobe, Shawn M., Katina M. Wilson, Lori Leo, Jeffery D. Molkentin, Steven R. Lentz, and Jorge Di Paola. "Critical Role for Cyclophilin D and the Mitochondrial Permeability Transition Pore (MPTP) in Platelet Activation." Blood 108, no. 11 (2006): 1508. http://dx.doi.org/10.1182/blood.v108.11.1508.1508.

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Abstract Dual stimulation of platelets with thrombin and collagen results in the formation of a unique subpopulation of highly activated platelets. Characteristics of the highly activated platelet subpopulation includeincreased surface retention of procoagulant alpha granule proteins,high-level phosphatidylserine (PS) externalization, andmodulation of the fibrinogen receptor αIIbβ3 as evidenced by their decreased recognition by antibodies to activated αIIbβ3 such as PAC-1 and JON/A. Formation of the highly activated platelet subpopulation is closely correlated with a rapid loss of mitochondria

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Gaunt, Stephen D., Dale C. Baker, and Shirley S. Babin. "Platelet aggregation studies in dogs with acute Ehrlichia platys infection." American Journal of Veterinary Research 51, no. 2 (1990): 290–93. http://dx.doi.org/10.2460/ajvr.1990.51.02.290.

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SUMMARY Ten adult dogs (5 Beagles and 5 mixed-breed dogs) were inoculated IV with canine platelets containing Ehrlichia platys. Inclusions and morulae of E platys developed in platelets of infected dogs at 10 to 14 days after inoculation, followed by marked thrombocytopenia at 14 to 21 days. Parasitemia and marked thrombocytopenia recurred at 24 to 28 days after inoculation. Increased numbers of megakaryocytes were observed in marrow aspirate smears from infected dogs, indicative of regenerative thrombocytopenia. Prior to infection, platelet-rich plasma from these dogs was determined to have s

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32

Zhao, Xuefei, Matthew Cooper, Yanki Yanman, et al. "GRK2 Regulates ADP Signaling in Platelets Via P2Y 1 and P2Y 12." Blood 138, Supplement 1 (2021): 578. http://dx.doi.org/10.1182/blood-2021-148615.

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Abstract Abstract Venous thromboembolism (VTE), heart attack, and stroke are all diseases in which platelets play a role, through inappropriate platelet activation and subsequent thrombus formation. Most platelet agonists activate platelets via G protein-coupled receptors (GPCRs), which are targeted by many antiplatelet drugs. Along with thrombin and TxA 2, ADP has long been recognized for its important role in hemostasis and thrombosis. It activates platelets via GPCRs, P2Y 1 and P2Y 12. However, little is known about the negative feedback mechanisms governing P2Y receptor-mediated platelet a

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Winskel-Wood, Ben, Denese C. Marks, and Lacey Johnson. "Storage Temperature Affects Platelet Activation and Degranulation in Response to Stimuli." International Journal of Molecular Sciences 26, no. 7 (2025): 2944. https://doi.org/10.3390/ijms26072944.

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The refrigeration (cold storage) of platelet components provides several benefits over room-temperature (RT) storage, extending the shelf-life up to 21 days. However, the effect of storage conditions on platelet activation in response to stimulation remains unclear. A paired study was conducted where buffy-coat platelet concentrates were pooled, split, and allocated to RT or cold storage (n = 6 in each group). Platelet samples were taken on days 1, 7, 14, and 21, which were tested without stimulation or following activation with TRAP-6, A23187, lipopolysaccharides, or Histone-H4. Imaging flow

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34

Koupenova, Milka, Alison C. Livada, and Craig N. Morrell. "Platelet and Megakaryocyte Roles in Innate and Adaptive Immunity." Circulation Research 130, no. 2 (2022): 288–308. http://dx.doi.org/10.1161/circresaha.121.319821.

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Classically, platelets have been described as the cellular blood component that mediates hemostasis and thrombosis. This important platelet function has received significant research attention for >150 years. The immune cell functions of platelets are much less appreciated. Platelets interact with and activate cells of all branches of immunity in response to pathogen exposures and infection, as well as in response to sterile tissue injury. In this review, we focus on innate immune mechanisms of platelet activation, platelet interactions with innate immune cells, as well as the intersection

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35

Hurley, Sinéad M., Fredrik Kahn, Pontus Nordenfelt, Matthias Mörgelin, Ole E. Sørensen, and Oonagh Shannon. "Platelet-Dependent Neutrophil Function Is Dysregulated by M Protein from Streptococcus pyogenes." Infection and Immunity 83, no. 9 (2015): 3515–25. http://dx.doi.org/10.1128/iai.00508-15.

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Platelets are rapidly responsive sentinel cells that patrol the bloodstream and contribute to the host response to infection. Platelets have been reported to form heterotypic aggregates with leukocytes and may modulate their function. Here, we have investigated platelet-neutrophil complex formation and neutrophil function in response to distinct agonists. The endogenous platelet activator thrombin gave rise to platelet-dependent neutrophil activation, resulting in enhanced phagocytosis and bacterial killing.Streptococcus pyogenesis an important causative agent of severe infectious disease, whi

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Park, Jin-Woo, Sang-Hyeob Han, and Takao Hanawa. "Effects of Surface Nanotopography and Calcium Chemistry of Titanium Bone Implants on Early Blood Platelet and Macrophage Cell Function." BioMed Research International 2018 (July 4, 2018): 1–10. http://dx.doi.org/10.1155/2018/1362958.

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Early responses of blood platelets and immunoinflammatory cells (macrophages) to titanium (Ti) bone implants affect the subsequent biological healing of implants by modulating early tissue healing-microenvironments via the formation of temporary fibrin matrix scaffolds for stem cell migration and production of growth factors and cytokines. This study investigated the effects of nanoscale surface topography and calcium ion (Ca2+) modification of Ti surfaces on biocompatibility regulated by blood platelets and macrophages, for the future surface design of Ti bone implants with enhanced early ost

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Utterback, P. J., and S. C. Hand. "Yolk platelet degradation in preemergence Artemia embryos: response to protons in vivo and in vitro." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 4 (1987): R774—R781. http://dx.doi.org/10.1152/ajpregu.1987.252.4.r774.

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Alteration of intracellular pH (pHi) influences yolk platelet degradation during preemergence development in Artemia embryos. Cysts incubated for 10 h under conditions of aerobic development (aqueous medium equilibrated with 60% N2-40% O2, pHi greater than or equal to 7.9) exhibit a significant decrease in numbers of yolk platelets and platelet protein. In contrast, cysts incubated for 10 h under aerobic acidosis (60% CO2-40% O2, pHi = 6.8) show no significant decrease in numbers of yolk platelets or platelet protein. When subjected to alkaline conditions in vitro, yolk platelets release prote

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Jackson, Shaun P., and Simone M. Schoenwaelder. "Procoagulant platelets: are they necrotic?" Blood 116, no. 12 (2010): 2011–18. http://dx.doi.org/10.1182/blood-2010-01-261669.

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AbstractApoptosis and necrosis represent distinct cell death processes that regulate mammalian development, physiology and disease. Apoptosis characteristically leads to the silent destruction and removal of cells in the absence of an inflammatory response. In contrast, necrotic cell death can induce physiologic inflammatory responses linked to tissue defense and repair. Although anucleate, platelets undergo programmed cell death, with apoptosis playing an important role in clearing effete platelets from the circulation. While it has long been recognized that procoagulant platelets exhibit cha

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Bussel, James B., Andrew L. Frelinger, William B. Mitchell, et al. "Platelet Function and Response to Thrombopoietin Mimetics In Wiskott-Aldrich Syndrome/X-Linked Thrombocytopenia." Blood 116, no. 21 (2010): 1429. http://dx.doi.org/10.1182/blood.v116.21.1429.1429.

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Abstract Abstract 1429 Introduction: Wiskott-Aldrich syndrome (WAS) is a complex disease in which patients suffer from both bleeding and immunodeficiency. Thrombocytopenia is severe, platelets are small and may be dysfunctional; intracranial hemorrhage occurs in 20% of patients. In patients with the full WAS phenotype, early use of human stem cell transplantation (HSCT) corrects the immune deficiency and thrombocytopenia although platelet transfusions are often required. Bleeding is the main complication of the X-linked thrombocytopenia (XLT) form, whose management may include HSCT, splenectom

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Burgess-Wilson, ME, SR Cockbill, GI Johnston, and S. Heptinstall. "Platelet aggregation in whole blood from patients with Glanzmann's thrombasthenia." Blood 69, no. 1 (1987): 38–42. http://dx.doi.org/10.1182/blood.v69.1.38.38.

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Abstract We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood from two patients with Glanzmann's thrombasthenia. In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to aggregating agents; to measure platelet aggregation in whole blood, we used a platelet counting technique. In PRP, the patients' platelets showed defective aggregation in response to ADP, adrenaline, arachidonic acid (AA), and collagen, but normal agglutination occurred in response to ristocetin. In whole blood, however, platelet aggregation in res

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Burgess-Wilson, ME, SR Cockbill, GI Johnston, and S. Heptinstall. "Platelet aggregation in whole blood from patients with Glanzmann's thrombasthenia." Blood 69, no. 1 (1987): 38–42. http://dx.doi.org/10.1182/blood.v69.1.38.bloodjournal69138.

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We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood from two patients with Glanzmann's thrombasthenia. In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to aggregating agents; to measure platelet aggregation in whole blood, we used a platelet counting technique. In PRP, the patients' platelets showed defective aggregation in response to ADP, adrenaline, arachidonic acid (AA), and collagen, but normal agglutination occurred in response to ristocetin. In whole blood, however, platelet aggregation in response to

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Wells, Lidia M. M., Oscar C. Mena, Shahajahan J. Chowdhury, Joseph D. Gheorghe, Udochukwu Oyoyo, and Danilo S. Boskovic. "Lipopolysaccharide from Proteus mirabilis Slows Platelet Plug Formation in Human Whole Blood." Bacteria 3, no. 4 (2024): 358–68. http://dx.doi.org/10.3390/bacteria3040024.

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Platelets are well known for their role in hemostasis. Additionally, platelets play a crucial role in immune and inflammatory responses. Toll-like receptors (TLRs) can mediate bacterial interactions during infection, triggering platelets to initiate an inflammatory response. TLR-4 receptors enable direct interactions between platelets and the bacterial lipopolysaccharide (LPS) endotoxin. The aim of this study was to assess platelet plug formation in response to LPS from Proteus mirabilis. Human whole blood was treated with varying concentrations of LPS over a range of incubation times. Then, p

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Provenzale, Isabella, Ilaria De Simone, Jonathan M. Gibbins, Johan W. M. Heemskerk, Paola E. J. van der Meijden, and Chris I. Jones. "Regulation of Glycoprotein VI-Dependent Platelet Activation and Thrombus Formation by Heparan Sulfate Proteoglycan Perlecan." International Journal of Molecular Sciences 24, no. 17 (2023): 13352. http://dx.doi.org/10.3390/ijms241713352.

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Proteoglycans form a heterogeneous family of proteins with covalently bound sulfated glycosaminoglycans. The extracellular matrix proteoglycan perlecan has been proposed to bind to the platelet- and megakaryocyte-specific receptor G6bB, co-regulating platelet glycoprotein VI (GPVI) signaling. The derived non-sulfate proteoglycan endorepellin was previously shown to enhance platelet adhesion via the collagen receptor, integrin α2β1. Here, we compared the roles of perlecan and other matrix proteoglycans in platelet responses and thrombus formation. We used multi-color flow cytometry to measure t

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Chaudhary, Preeti Kumari, Sanggu Kim, Youngheun Jee, Seung-Hun Lee, Kyung-Mee Park, and Soochong Kim. "Role of GRK6 in the Regulation of Platelet Activation through Selective G Protein-Coupled Receptor (GPCR) Desensitization." International Journal of Molecular Sciences 21, no. 11 (2020): 3932. http://dx.doi.org/10.3390/ijms21113932.

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Platelet G protein-coupled receptors (GPCRs) regulate platelet function by mediating the response to various agonists, including adenosine diphosphate (ADP), thromboxane A2, and thrombin. Although GPCR kinases (GRKs) are considered to have the crucial roles in most GPCR functions, little is known regarding the regulation of GPCR signaling and mechanisms of GPCR desensitization by GRKs in platelets. In this study, we investigated the functional role of GRK6 and the molecular basis for regulation of specific GPCR desensitization by GRK6 in platelets. We used GRK6 knockout mice to evaluate the fu

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Ruan, CG, XP Du, XD Xi, PA Castaldi, and MC Berndt. "A murine antiglycoprotein Ib complex monoclonal antibody, SZ 2, inhibits platelet aggregation induced by both ristocetin and collagen." Blood 69, no. 2 (1987): 570–77. http://dx.doi.org/10.1182/blood.v69.2.570.570.

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Abstract A new monoclonal antibody (MoAb), SZ 2, reactive with the human platelet glycoprotein Ib complex has been produced by the hybridoma technique. SZ 2 immunoprecipitated the components of the glycoprotein Ib complex, glycoprotein Ib and glycoprotein IX, from Triton-X-100- solubilized, periodate-labeled platelets. Western blot analysis indicated that the epitope for SZ 2 was on the alpha-subunit of glycoprotein Ib. Scatchard analysis of SZ 2 binding to formaldehyde- fixed, washed platelets revealed a single class of binding sites with Kd = 6.6 +/- 3.3 X 10(-10) mol/L and 15,200 +/- 4,100

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Ruan, CG, XP Du, XD Xi, PA Castaldi, and MC Berndt. "A murine antiglycoprotein Ib complex monoclonal antibody, SZ 2, inhibits platelet aggregation induced by both ristocetin and collagen." Blood 69, no. 2 (1987): 570–77. http://dx.doi.org/10.1182/blood.v69.2.570.bloodjournal692570.

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A new monoclonal antibody (MoAb), SZ 2, reactive with the human platelet glycoprotein Ib complex has been produced by the hybridoma technique. SZ 2 immunoprecipitated the components of the glycoprotein Ib complex, glycoprotein Ib and glycoprotein IX, from Triton-X-100- solubilized, periodate-labeled platelets. Western blot analysis indicated that the epitope for SZ 2 was on the alpha-subunit of glycoprotein Ib. Scatchard analysis of SZ 2 binding to formaldehyde- fixed, washed platelets revealed a single class of binding sites with Kd = 6.6 +/- 3.3 X 10(-10) mol/L and 15,200 +/- 4,100 binding s

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Wang, Zhangfei, Man Fang, Juan Li, Ruining Yang, Jianping Du, and Yiqin Luo. "High Platelet Levels Attenuate the Efficacy of Platinum-Based Treatment in Non-Small Cell Lung Cancer." Cellular Physiology and Biochemistry 48, no. 6 (2018): 2456–69. http://dx.doi.org/10.1159/000492683.

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Background/Aims: The correlation between platelet levels and clinical outcomes has received increasing attention, but it is not yet clear whether and how platelet levels affect the therapeutic response in non-small cell lung cancer (NSCLC). In the current study, we aimed to explore the role of platelet levels in responsive to platinum-based chemotherapy and investigated the underlying mechanism. Methods: We evaluated the possibility of platelet level as a biomarker for response to platinum-based therapy in NSCLC by retrospective analysis of NSCLC patients. Cell proliferation was evaluated usin

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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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Melford, S. K., C. M. Bunce, J. Gibbins, S. P. Watson, and J. C. Mountford. "Collagen or Collagen-related Peptide Cause [Ca2+]i Elevation and Increased Tyrosine Phosphorylation in Human Megakaryocytes." Thrombosis and Haemostasis 82, no. 09 (1999): 1153–59. http://dx.doi.org/10.1055/s-0037-1614345.

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SummarySince megakaryocytes are the cellular precursors of platelets we have investigated whether they share responses to platelet agonists, in particular collagen. Although previous studies have reported responses to thrombin in non-human megakaryocytes, through studies of single cell calcium responses and protein tyrosine-phosphorylation we demonstrate for the first time that both isolated human megakaryocytes and CD41/61-positive megakaryocytes derived in culture from CD34+ cells share responses to the platelet agonists collagen, collagen-related peptide and thrombin. The responses to eithe

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Bracamonte, M. P., K. S. Rud, Whyte G. Owen, and V. M. Miller. "Ovariectomy increases mitogens and platelet-induced proliferation of arterial smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 3 (2002): H853—H860. http://dx.doi.org/10.1152/ajpheart.00201.2002.

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Experiments were designed to determine how ovariectomy modulates mitogenic factors in platelets and how these factors affect proliferation of coronary arterial smooth muscle. Platelet-derived growth factors (PDGFABand PDGFBB), transforming growth factors (TGF-β1and TGF-β2), and vascular endothelial growth factor (VEGF165) were quantified in platelet lysates and platelet-poor plasma from adult gonadally intact and ovariectomized female pigs by ELISA. Proliferation of cultured coronary arterial smooth muscle cells (SMCs) from both groups of pigs was determined in response to autologous or hetero

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