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Articoli di riviste sul tema "Platelets"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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1

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

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

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2

Franco, Aime T., Adam Corken, and Jerry Ware. "Platelets at the interface of thrombosis, inflammation, and cancer." Blood 126, no. 5 (2015): 582–88. http://dx.doi.org/10.1182/blood-2014-08-531582.

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Abstract Although once primarily recognized for its roles in hemostasis and thrombosis, the platelet has been increasingly recognized as a multipurpose cell. Indeed, circulating platelets have the ability to influence a wide range of seemingly unrelated pathophysiologic events. Here, we highlight some of the notable observations that link platelets to inflammation, reinforcing the platelet’s origin from a lower vertebrate cell type with both hemostatic and immunologic roles. In addition, we consider the relevance of platelets in cancer biology by focusing on the hallmarks of cancer and the way

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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

Campbell, Robert A., Thomas H. Fischer, and Alisa S. Wolberg. "Rehydrated, Lyophilized Platelets Generate Thrombin in the Presence of Recombinant Factor VIIa." Blood 106, no. 11 (2005): 4057. http://dx.doi.org/10.1182/blood.v106.11.4057.4057.

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Abstract The anti-bleeding therapy, recombinant factor VIIa (rFVIIa), is thought to bind to the platelet’s surface and increase thrombin generation in hemophilia. However, high plasma levels of rFVIIa are required, in part, due to the weak binding of rFVIIa to platelets. We hypothesized that the efficacy of the therapy could be improved by administering rFVIIa already bound to platelets. A recently described protocol involving pretreatment of platelets with paraformaldehyde permits platelets to be lyophilized while preserving many platelet functions. Such platelets could be used for binding rF

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5

Yang, Linlin, Roger Ottenheijm, Paul Worley, Marc Freichel, and Juan E. Camacho Londoño. "Reduction in SOCE and Associated Aggregation in Platelets from Mice with Platelet-Specific Deletion of Orai1." Cells 11, no. 20 (2022): 3225. http://dx.doi.org/10.3390/cells11203225.

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Calcium signalling in platelets through store operated Ca2+ entry (SOCE) or receptor-operated Ca2+ entry (ROCE) mechanisms is crucial for platelet activation and function. Orai1 proteins have been implicated in platelet’s SOCE. In this study we evaluated the contribution of Orai1 proteins to these processes using washed platelets from adult mice from both genders with platelet-specific deletion of the Orai1 gene (Orai1flox/flox; Pf4-Cre termed as Orai1Plt-KO) since mice with ubiquitous Orai1 deficiency show early lethality. Platelet aggregation as well as Ca2+ entry and release were measured i

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6

Smith, Clark M., Steven M. Burris, Douglas J. Weiss, and James G. White. "Comparison of bovine and human platelet deformability, using micropipette elastimetry." American Journal of Veterinary Research 50, no. 1 (1989): 34–38. https://doi.org/10.2460/ajvr.1989.50.01.34.

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SUMMARY We evaluated the deformability of bovine platelets and contrasted the effects of pharmacologic and thermal perturbations on cytoskeletal structure of human and bovine platelets. Platelets were aspirated into micropipettes (0.7 to 0.8 μm in diameter) by stepwise increments in tension. The resulting lengths of the cell extensions were recorded. The cell extensions aspirated from bovine platelets were shorter than the extensions drawn from human platelelets. Disassembly of the circumferential microtubule coil allowed human platelets to pass through the pipette, but the same treatments onl

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7

Crawford, N., A. Chajara, G. Pfliegler, B. EI Gamal, L. Brewer, and L. Capron. "Targeting Platelets Containing Electro-encapsulated lloprost to Balloon Injured Aorta in Rats." Thrombosis and Haemostasis 73, no. 03 (1995): 535–42. http://dx.doi.org/10.1055/s-0038-1653809.

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SummaryDrugs can be electro-encapsulated within platelets and targeted to damaged blood vessels by exploiting the platelet’s natural haemostatic properties to adhere to collagen and other vessel wall constituents revealed by injury. A rat aorta balloon angioplasty model has been used to study the effect on platelet deposition of giving iloprost loaded platelets i.v. during the balloon injury. After labelling the circulating platelets with 111-Indium before balloon injury, time course studies showed maximum platelet deposition on the injured aorta occurred at about 1 h post-injury and the depos

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8

Battinelli, Elisabeth M. "Platelet and Megakaryocytic Regulation of Tumor Progression." Blood 130, Suppl_1 (2017): SCI—26—SCI—26. http://dx.doi.org/10.1182/blood.v130.suppl_1.sci-26.sci-26.

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Traditionally viewed as the bandaids of the blood, the contribution of platelets to the progression of malignancy is emerging as a compelling focus for therapeutic intervention. Complex interactions between tumor cells, and circulating platelets play an important role in tumor growth and dissemination, and a growing body of data supports a role for platelet activation and release of chemokines in metastases and neovascularization. Supporting this concept is the evidence that elevated platelet counts (thrombocytosis) at time of diagnosis with malignancy is a harbinger of an aggressive cancer wi

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9

Puricelli, Chiara, Elena Boggio, Casimiro Luca Gigliotti, et al. "Platelets, Protean Cells with All-Around Functions and Multifaceted Pharmacological Applications." International Journal of Molecular Sciences 24, no. 5 (2023): 4565. http://dx.doi.org/10.3390/ijms24054565.

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Platelets, traditionally known for their roles in hemostasis and coagulation, are the most prevalent blood component after erythrocytes (150,000–400,000 platelets/μL in healthy humans). However, only 10,000 platelets/μL are needed for vessel wall repair and wound healing. Increased knowledge of the platelet’s role in hemostasis has led to many advances in understanding that they are crucial mediators in many other physiological processes, such as innate and adaptive immunity. Due to their multiple functions, platelet dysfunction is involved not only in thrombosis, mediating myocardial infarcti

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10

Cheepala, Satish B., Kazumasa Takenaka, Tamara I. Pestina, Carl W. Jackson, and John D. Schuetz. "The Role of ABC Transporter Abcc4 in Platelets Physiologic Function and Its Impact On Collagen Meditated Platelet Aggregation." Blood 120, no. 21 (2012): 1063. http://dx.doi.org/10.1182/blood.v120.21.1063.1063.

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Abstract Abstract 1063 Platelet activation is a highly regulated process, and cyclic nucleotide mediated signaling pathways are crucial to effective platelet activation. Vascular injury produces, exposed collagen which binds circulating platelets through the platelet's “collagen” receptor, GPVI, resulting in the activation of guanyly/adenlyl cyclases. These interactions result in the rapid alterations in the cyclic nucleotide concentration inside the platelets leading to activation of protein kinase A and G signaling pathways to modulate platelet function. While, ABCC4 functions as a plasma me

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11

Ismail, M. Taufik. "Distinct Mechanism between Arterial and Venous Thrombosis: Impact for Clinical Manifestations." ACI (Acta Cardiologia Indonesiana) 5, no. 1 (P) (2019): 47. http://dx.doi.org/10.22146/aci.47683.

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Hemostasis is a complex physiological process aiming to keep the integrity of a closed circulatory system after an occurrence of vessel wall injury. Hemostasis involving the role of circulating platelets and coagulation cascade.1 There are two major pathways that act independently to activate the platelet. The first pathway is mediated by collagen and the other by tissue factor. After intimal layer injury, platelets are recruited through the interaction between platelet’s surface glycoprotein (GPVI and GPIb/V/IX) with collagen and von Willebrand factor. This process results in adhesion of plat

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12

Battinelli, Elisabeth M., Rajesh Kulenthirarajan, Joseph E. Italiano, and Kelly Johnson. "Tamoxifen Directly Disrupts Platelet Angiogenic Potential and Inhibits Platelet-Mediated Metastasis." Blood 124, no. 21 (2014): 4169. http://dx.doi.org/10.1182/blood.v124.21.4169.4169.

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Abstract Platelets, which are mainly known for their role in hemostasis, are now known to play a crucial role in metastasis. Metastatic disease is the cause of roughly 90% of all cancer-related deaths and understanding the mechanisms leading to dissemination of tumor cells to distant sites remains one of the main challenges of cancer research. Tamoxifen is a selective estrogen receptor modulator that is widely used for the treatment and prevention of breast cancer. Interestingly, tamoxifen has demonstrated anti-cancer efficacy in estrogen negative breast cancers suggesting that this drug has a

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13

SANTORO, S. A. "Platelets: Platelet Immunobiology." Science 245, no. 4915 (1989): 314–15. http://dx.doi.org/10.1126/science.245.4915.314.

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14

Lievens, Dirk, Alma Zernecke, Tom Seijkens, et al. "Platelet CD40L mediates thrombotic and inflammatory processes in atherosclerosis." Blood 116, no. 20 (2010): 4317–27. http://dx.doi.org/10.1182/blood-2010-01-261206.

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Abstract CD40 ligand (CD40L), identified as a costimulatory molecule expressed on T cells, is also expressed and functional on platelets. We investigated the thrombotic and inflammatory contributions of platelet CD40L in atherosclerosis. Although CD40L-deficient (Cd40l−/−) platelets exhibited impaired platelet aggregation and thrombus stability, the effects of platelet CD40L on inflammatory processes in atherosclerosis were more remarkable. Repeated injections of activated Cd40l−/− platelets into Apoe−/− mice strongly decreased both platelet and leukocyte adhesion to the endothelium and decrea

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15

He, Ao-Di, Ming-Lu Liang, Gang Liu та ін. "The Role of FcγRIIa and TGF-β1/KLF6 Pathway in Platelet's Promoting Hepatocellular Carcinoma Cells Growth". Blood 124, № 21 (2014): 1429. http://dx.doi.org/10.1182/blood.v124.21.1429.1429.

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Abstract Background: Platelet in the primary tumor microenvironment plays a crucial role in tumor cells angiogenesis, growth, and metastasis. Clinical and experimental evidences support that platelets and their extracts influence hepatocellular carcinoma (HCC) growth and biology. But the mechanism is still not fully clarified. The aim of present study was to elucidate an unperceived mechanism of the proliferative effect of platelet on HCC cells. Methods: Human blood was collected from health volunteers, washed platelets were prepared and resuspended by fresh medium. The ability of HepG2 cells

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16

Parker, RI, and HR Gralnick. "Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets." Blood 74, no. 6 (1989): 2016–21. http://dx.doi.org/10.1182/blood.v74.6.2016.2016.

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Abstract Platelets contain a pool of endogenous platelet-von Willebrand factor (vWF) that becomes expressed on the platelet surface when platelets are stimulated by a variety of agonists. Maximal platelet-vWF expression occurs in concert with platelet alpha-granule secretion. Aspirin (ASA) is known to impair platelet activation and alpha-granule secretion by irreversible inhibition of platelet cyclo-oxygenase. We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin. We found that each agonist w

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Parker, RI, and HR Gralnick. "Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets." Blood 74, no. 6 (1989): 2016–21. http://dx.doi.org/10.1182/blood.v74.6.2016.bloodjournal7462016.

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Abstract (sommario):

Platelets contain a pool of endogenous platelet-von Willebrand factor (vWF) that becomes expressed on the platelet surface when platelets are stimulated by a variety of agonists. Maximal platelet-vWF expression occurs in concert with platelet alpha-granule secretion. Aspirin (ASA) is known to impair platelet activation and alpha-granule secretion by irreversible inhibition of platelet cyclo-oxygenase. We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin. We found that each agonist was effect

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Sakurai, Yumiko, Jennifer L. Fitch-Tewfik, Yongzhi Qiu та ін. "“Self-Deposition” of Matrix Proteins from Platelet α-Granules Enable Extended Adhesion and Spreading on Micron/Submicron-Scale Fibrinogen and Collagen Substrates." Blood 124, № 21 (2014): 2764. http://dx.doi.org/10.1182/blood.v124.21.2764.2764.

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Abstract Introduction: While the platelet’s role in achieving hemostasis in the context of bleeding is well-characterized, how platelets support and maintain vascular integrity during homeostatic, non-thrombotic conditions remains unclear. Previous studies have shown that single platelets fill micron/submicron-sized “gaps” of small discontinuities in the endothelium. In this context, however, as the overall force of adhesion correlates with the area of exposed subendothelial matrix, how platelets establish sufficient adhesion to resist the dynamic shear forces of the circulation are unknown. I

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19

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

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

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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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Hoffmann, Johannes J. M. L., Nicole M. A. van den Broek, and Joyce Curvers. "Reference Intervals of Reticulated Platelets and Other Platelet Parameters and Their Associations." Archives of Pathology & Laboratory Medicine 137, no. 11 (2013): 1635–40. http://dx.doi.org/10.5858/arpa.2012-0624-oa.

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Context.—Reticulated platelets are platelets recently released from the bone marrow, and they can serve as a noninvasive indicator of recent megakaryopoietic activity. Widespread clinical use has been hampered by laborious methods and lack of standardization. Recently, a fully automated method was released on the Abbott CELL-DYN Sapphire hematology analyzer. Objective.—To establish reference ranges for reticulated platelets. Secondary aims were to investigate associations between reticulated platelets and other platelet parameters like mean platelet volume, plateletcrit, and platelet distribut

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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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Fager, Ammon M., and Paula B. Tracy. "“Young” Platelets Regulate Thrombus Formation by Expression of Increased Adhesive Properties and Procoagulant Activity." Blood 108, no. 11 (2006): 1527. http://dx.doi.org/10.1182/blood.v108.11.1527.1527.

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Abstract Previous studies from our lab and others have demonstrated that thrombin mediated activation of platelets results in the formation of a distinct procoagulant subpopulation capable of assembling the components of both the prothrombinase complex and intrinsic tenase complex at its surface. A similar subpopulation has been identified following activation of platelets with the combination of thrombin and convulxin, a glycoprotein VI agonist, and has been found to be enriched in young platelets. In addition, young zebrafish thrombocytes were shown to have a higher density of adhesive recep

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Liu, Fang, Graciela Gamez, David R. Myers, Wilbur Lam, and Shawn M. Jobe. "Mitochondrially-Mediated Platelet Integrin AlphaIIbbeta3 Inactivation Limits Platelet Recruitment and Thrombus Growth,." Blood 118, no. 21 (2011): 3251. http://dx.doi.org/10.1182/blood.v118.21.3251.3251.

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Abstract Abstract 3251 Platelet stimulation with strong agonist(s) results in the formation of a phenotypically unique platelet subpopulation known as procoagulant platelets. All platelets stimulated in strongly-activating conditions undergo granule release, activation of integrin αIIbβ3, and spreading. However, minutes later a subpopulation of these activated platelets undergo additional phenotypic changes including phosphatidylserine (PS) exposure, adoption of a vesiculated and balloon-like morphology, and an altered integrin αIIbβ3 conformation that has a decreased binding affinity for acti

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Maurya, Preeti, Sara Ture, Kathleen E. McGrath, James Palis, and Craig N. Morrell. "Adult, but Not Neonatal, Platelet Transfusions Drive a Monocyte Trafficking Phenotype in Vitro and In Vivo." Blood 138, Supplement 1 (2021): 2144. http://dx.doi.org/10.1182/blood-2021-152913.

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Abstract Although, thrombocytopenia can affect all age groups, neonates, especially pre-term, have an increased incidence of thrombocytopenia. Platelet transfusions may reduce the bleeding risk in neonates, but are also associated with adverse short and long-term immune and inflammatory outcomes. A randomized trial of platelet transfusions in neonates found that transfusion was associated with an increased risk of necrotizing enterocolitis, unilateral/bilateral retinopathy, and bronchopulmonary dysplasia. Past work from our research team found that neonatal platelets expressed lower levels of

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Lominadze, David G., Jack T. Saari, Frederick N. Miller, James L. Catalfamo, David E. Justus, and Dale A. Schuschke. "Platelet Aggregation and Adhesion during Dietary Copper Deficiency in Rats." Thrombosis and Haemostasis 75, no. 04 (1996): 630–34. http://dx.doi.org/10.1055/s-0038-1650334.

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SummaryThe role of dietary copper deficiency in platelet-to-endothelial cell adhesion and in platelet-to-platelet aggregation was studied in vitro. Platelets were obtained from male, weanling Sprague-Dawley rats fed purified diets which were either copper-adequate (CuA, 6.3 μg copper/g of diet) or copper-deficient (CuD, 0.3 μg copper/g of diet) for 4 weeks. The platelet adhesion study was performed by adding CuA or CuD platelets either suspended in homologous plasma or in Tyrode buffer salt solution (TBSS) to cultured rat endothelial cells. After a one hour incubation at 37° C non-adhered plat

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Sen Gupta, Anirban. "Synthetic Platelets for Treatment of Traumatic Hemorrhage and Thrombocytopenia." Blood 134, Supplement_1 (2019): SCI—37—SCI—37. http://dx.doi.org/10.1182/blood-2019-121079.

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Platelets are primarily responsible for staunching bleeding by forming a 'platelet plug' and further amplifying thrombin generation on its surface to facilitate fibrin formation, leading to hemostatic clot formation at the site of vascular breach. Therefore, platelet transfusions are clinically used to mitigate bleeding risks in thrombocytopenia (prophylactic transfusion) and to mitigate hemorrhage in traumatic injuries (emergency transfusion). Currently these transfusions utilize donor-derived platelets, stored at 20-24oC with gentle agitation. In this condition, platelets have high risk of b

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Savage, B., CS Hunter, LA Harker, VL Jr Woods, and SR Hanson. "Thrombin-induced increase in surface expression of epitopes on platelet membrane glycoprotein IIb/IIIa complex and GMP-140 is a function of platelet age." Blood 74, no. 3 (1989): 1007–14. http://dx.doi.org/10.1182/blood.v74.3.1007.1007.

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Abstract Platelets are heterogeneous in the content of membrane glycoprotein (GP)IIb/IIIa complex. To determine whether this heterogeneity is related to changes associated with platelet aging in the circulation, newly released platelets, obtained during recovery from nonimmune- mediated acute experimental thrombocytopenia in baboons, were studied. Monoclonal antibody (MoAb) binding to epitopes expressed on GPIIb/IIIa complex (LJ-CP8), GMP-140 (S12), and GPIa/IIa (12F1) was measured on control platelets (comprising platelets with a normal age distribution; mean age 60 to 72 hours) and newly for

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Savage, B., CS Hunter, LA Harker, VL Jr Woods, and SR Hanson. "Thrombin-induced increase in surface expression of epitopes on platelet membrane glycoprotein IIb/IIIa complex and GMP-140 is a function of platelet age." Blood 74, no. 3 (1989): 1007–14. http://dx.doi.org/10.1182/blood.v74.3.1007.bloodjournal7431007.

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Platelets are heterogeneous in the content of membrane glycoprotein (GP)IIb/IIIa complex. To determine whether this heterogeneity is related to changes associated with platelet aging in the circulation, newly released platelets, obtained during recovery from nonimmune- mediated acute experimental thrombocytopenia in baboons, were studied. Monoclonal antibody (MoAb) binding to epitopes expressed on GPIIb/IIIa complex (LJ-CP8), GMP-140 (S12), and GPIa/IIa (12F1) was measured on control platelets (comprising platelets with a normal age distribution; mean age 60 to 72 hours) and newly formed plate

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Savage, B., PR McFadden, SR Hanson, and LA Harker. "The relation of platelet density to platelet age: survival of low- and high-density 111indium-labeled platelets in baboons." Blood 68, no. 2 (1986): 386–93. http://dx.doi.org/10.1182/blood.v68.2.386.386.

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Abstract The relationship between platelet density and platelet age has been studied using continuous linear Percoll density gradients and 111In- labeling of autologous platelets in baboons. To investigate changes in platelet density during senescence in the circulation, baboons were infused with 111In-labeled autologous platelets, and blood was collected at one hour postinfusion and twice daily thereafter for six days. Platelets were isolated from these samples in high yield (greater than 95%) and separated in continuous linear Percoll density gradients following density equilibrium centrifug

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Savage, B., PR McFadden, SR Hanson, and LA Harker. "The relation of platelet density to platelet age: survival of low- and high-density 111indium-labeled platelets in baboons." Blood 68, no. 2 (1986): 386–93. http://dx.doi.org/10.1182/blood.v68.2.386.bloodjournal682386.

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The relationship between platelet density and platelet age has been studied using continuous linear Percoll density gradients and 111In- labeling of autologous platelets in baboons. To investigate changes in platelet density during senescence in the circulation, baboons were infused with 111In-labeled autologous platelets, and blood was collected at one hour postinfusion and twice daily thereafter for six days. Platelets were isolated from these samples in high yield (greater than 95%) and separated in continuous linear Percoll density gradients following density equilibrium centrifugation. Al

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Zhao, Xi, Yangchao Zhao, Yanzhong Ding, et al. "Autophagy Ameliorates Reactive Oxygen Species-Induced Platelet Storage Lesions." Oxidative Medicine and Cellular Longevity 2022 (April 5, 2022): 1–11. http://dx.doi.org/10.1155/2022/1898844.

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Platelet transfusion is a life-saving therapy to prevent bleeding; however, the availability of platelets for transfusion is limited by the markedly short shelf life owing to the development of platelet storage lesions (PSLs). The mechanism of PSLs remains obscure. Dissection of the intracellular biological changes in stored platelets may help to reduce PSLs and improve platelet transfusion efficiency. In the present study, we explore the changes of stored platelets at room temperature under constant agitation. We found that platelets during storage showed an increased reactive oxygen species

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Pedersen, Oliver Buchhave, Leonardo Pasalic, Erik Lerkevang Grove, Steen Dalby Kristensen, Anne-Mette Hvas, and Peter H. Nissen. "Advanced Flow Cytometry Using the SYTO-13 Dye for the Assessment of Platelet Reactivity and Maturity in Whole Blood." Methods and Protocols 6, no. 1 (2023): 8. http://dx.doi.org/10.3390/mps6010008.

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Newly produced immature platelets are larger, contain higher amounts of residual RNA, and are more reactive than mature platelets. Flow cytometry using the SYTO-13 dye is a method for the subdivision of immature platelets from mature platelets based on the labelling of intracellular platelet RNA, enabling the simultaneous investigation of the reactivity of each platelet population. This method provides detailed information on several aspects of platelet physiology using a combination of platelet surface markers and agonists. Currently, no standardized protocol exists across laboratories. Here,

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Battinelli, Elisabeth M., Kelly Elizabeth Johnson, Jodi A. Forward, et al. "Tamoxifen Directly Inhibits Platelet Activation, Angiogenic Potential and Platelet-Mediated Metastasis." Blood 128, no. 22 (2016): 3723. http://dx.doi.org/10.1182/blood.v128.22.3723.3723.

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Abstract Objective - Platelets, which are mainly known for their role in hemostasis, are now known to play a crucial role in tumor metastasis and neovascularization. Metastatic disease is the cause of roughly 90% of all cancer-related deaths and understanding the mechanisms leading to dissemination of tumor cells to distant sites remains one of the main challenges of cancer research. Platelets carry a plethora of potent angiogenic and metastatic mediators within their alpha-granules and exposure to breast tumor cells induces platelet activation, leading to release of these mediators. Tamoxifen

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35

Campbell, Robert A., Thomas H. Fischer, and Alisa S. Wolberg. "A Novel Use of Rehydrated, Lyophilized Platelets Increases Recombinant FVIIa Procoagulant Activity in a Model of Hemophilia." Blood 108, no. 11 (2006): 1754. http://dx.doi.org/10.1182/blood.v108.11.1754.1754.

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Abstract The anti-bleeding therapy recombinant factor VIIa (rFVIIa) is used to abrogate bleeding in hemophiliacs with inhibitors, bypassing the need for replacement factors. RFVIIa is hypothesized to work by increasing Xa generation on the platelet’s surface. However, high plasma levels of rFVIIa are required, in part due to the weak binding of rFVIIa to platelets. We hypothesized that the efficacy of the therapy could be improved by administering rFVIIa already bound to platelets. One platelet preparative that may be used in this application is rehydrated, lyophilized (RL) platelets. RL plate

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36

Jacob, Shancy, Marina Tistao, Abigail Ajanel Gomez, et al. "Mitochondrial Fission Protein Drp1 Regulates Platelet Function." Blood 142, Supplement 1 (2023): 1201. http://dx.doi.org/10.1182/blood-2023-187556.

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Abstract (sommario):

Background: Mitochondria in platelets contribute to platelet function and are altered by diseases that involve dysregulated hemostasis or thrombosis. Mitochondrial integrity, governed by its size, number and distribution is modulated by fusion and fission proteins. Pharmacological inhibition of the mitochondrial fission protein Dynamin-related protein 1 (Drp1) has been shown to inhibit granule release in human platelets and impair thrombus formation in a murine model of thrombosis. However, the mitochondrial roles for Drp1 in platelet function are still largely unknown. Objective: To determine

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37

Marjanovic, Jasna A., Aleksandra Stojanovic, Viktor Brovkovych, Randal A. Skidgel, and Xiaoping Du. "Inducible Nitric Oxide Synthase Plays a Stimulatory Role in Platelet Activation." Blood 106, no. 11 (2005): 1650. http://dx.doi.org/10.1182/blood.v106.11.1650.1650.

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Abstract Platelets generate nitric oxide (NO) in response to agonist stimulation. Previous reports have shown that the endothelial nitric oxide synthase (eNOS) plays a role in agonist-stimulated platelet NO production and in platelet activation. Here we show that platelets from eNOS knockout mice (eNOS−/−) showed only partial reduction in thrombin-induced NO production compared to wild type platelets (50% reduction), indicating the presence of another NOS isoform in platelets. More importantly, we show that resting platelets express functional inducible nitric oxide synthase (iNOS), which part

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38

Yuhki, Koh-ichi, Fumiaki Kojima, Takehiro Yamada, et al. "Selective activation of the prostaglandin E2 receptor subtype EP2 or EP4 leads to inhibition of platelet aggregation." Thrombosis and Haemostasis 104, no. 10 (2010): 796–803. http://dx.doi.org/10.1160/th10-01-0043.

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Abstract (sommario):

SummaryThe effect of selective activation of platelet prostaglandin (PG) E2 receptor subtype EP2 or EP4 on platelet aggregation remains to be determined. In platelets prepared from wild-type mice (WT platelets), high concentrations of PGE2 inhibited platelet aggregation induced by U-46619, a thromboxane receptor agonist. However, there was no significant change in the inhibitory effect of PGE2 on platelets lacking EP2 (EP2 –/– platelets) and EP4 (EP4 –/– platelets) compared with the inhibitory effect on WT platelets. On the other hand, AE1–259 and AE1–329, agonists for EP2 and EP4, respectivel

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39

Goodnough, Lawrence T., David J. Kuter, Jeffrey McCullough, et al. "Prophylactic platelet transfusions from healthy apheresis platelet donors undergoing treatment with thrombopoietin." Blood 98, no. 5 (2001): 1346–51. http://dx.doi.org/10.1182/blood.v98.5.1346.

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Abstract (sommario):

Many patients receiving dose-intensive chemotherapy acquire thrombocytopenia and need platelet transfusions. A study was conducted to determine whether platelets harvested from healthy donors treated with thrombopoietin could provide larger increases in platelet counts and thereby delay time to next platelet transfusion compared to routinely available platelets given to thrombocytopenic patients. Community platelet donors received either 1 or 3 μg/kg pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) or placebo and then donated platelets 10 to 15 days later.

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40

Schmaier, AH, HN Bradford, D. Lundberg, A. Farber, and RW Colman. "Membrane expression of platelet calpain." Blood 75, no. 6 (1990): 1273–81. http://dx.doi.org/10.1182/blood.v75.6.1273.1273.

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Abstract (sommario):

Abstract Platelet calpain has many platelet substrates, including external membrane proteins. We thus investigated whether platelet calpain II was associated with platelet membranes in unstimulated and thrombin- activated platelets. A monospecific, goat polyclonal antibody was reared to purified platelet calpain II. Sixteen whole platelet lysates were found to contain 4.5 +/- 0.7 micrograms calpain antigen II per 10(8) platelets (mean +/- SEM) as determined by a competitive enzyme- linked immunosorbent assay. Using the dipeptide fluorogenic substrate, Suc-Leu-Tyr-MCA, 17 human platelet lysates

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41

Schmaier, AH, HN Bradford, D. Lundberg, A. Farber, and RW Colman. "Membrane expression of platelet calpain." Blood 75, no. 6 (1990): 1273–81. http://dx.doi.org/10.1182/blood.v75.6.1273.bloodjournal7561273.

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Abstract (sommario):

Platelet calpain has many platelet substrates, including external membrane proteins. We thus investigated whether platelet calpain II was associated with platelet membranes in unstimulated and thrombin- activated platelets. A monospecific, goat polyclonal antibody was reared to purified platelet calpain II. Sixteen whole platelet lysates were found to contain 4.5 +/- 0.7 micrograms calpain antigen II per 10(8) platelets (mean +/- SEM) as determined by a competitive enzyme- linked immunosorbent assay. Using the dipeptide fluorogenic substrate, Suc-Leu-Tyr-MCA, 17 human platelet lysates containe

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42

Jobe, Shawn M., Lorie Leo, Joshua S. Eastvold та ін. "Role of FcRγ and factor XIIIA in coated platelet formation". Blood 106, № 13 (2005): 4146–51. http://dx.doi.org/10.1182/blood-2005-03-1223.

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Abstract (sommario):

Platelet activation in response to dual stimulation with collagen and thrombin results in the formation of a subpopulation of activated platelets known as coated platelets. Coated platelets are characterized by high surface levels of α-granule proteins and phosphatidylserine, which support the assembly of procoagulant protein complexes. Using murine models, we tested the hypothesis that the collagen receptor-associated molecule FcRγ and the transglutaminase factor XIIIA are required for the formation of coated platelets. Following dual stimulation with the collagen receptor agonist convulxin a

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43

Charania, Roseleen, James W. Smith, Sara K. Vesely, George L. Dale, and Jennifer L. Holter. "Collection and Storage of Apheresis Platelets Results in a Significant Decline in the Percentage of Coated-Platelets." Blood 114, no. 22 (2009): 23. http://dx.doi.org/10.1182/blood.v114.22.23.23.

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Abstract (sommario):

Abstract Abstract 23 Introduction: Platelets initiate hemostasis by adhering to the site of vascular injury and providing a negatively charged surface for thrombin generation. A subset of platelets, referred to as coated-platelets, has an enhanced ability to generate thrombin. Coated-platelets, observed in vitro upon dual agonist stimulation with collagen and thrombin, retain several serotonin-derivatized proteins on their surface and express phosphotidylserine, creating a highly active prothrombinase complex. Experimental studies have concluded that dogs deficient in coated-platelets manifest

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44

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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Abstract (sommario):

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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45

Kim, Oleg V., Tatiana A. Nevzorova, Elmira R. Mordakhanova, et al. "Fatal Dysfunction and Fragmentation of Thrombin-Stimulated Platelets." Blood 132, Supplement 1 (2018): 521. http://dx.doi.org/10.1182/blood-2018-99-112703.

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Abstract (sommario):

Abstract Introduction: Platelets play a key role in formation of protective hemostatic blood clots and pathological obstructive thrombi. Under (patho)physiological conditions, chemically activated platelets change their morphology, express adhesive molecules, undergo aggregation, secrete procoagulant substances, and induce mechanical contraction (retraction) of the blood clots. Despite the vital importance of these platelet functions, the subsequent fate of activated platelets is largely unknown. We hypothesize that activated platelets undergo late alterations that determine their fate and may

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46

Tanoue, K., Y. Mano, K. Kuroiwa, H. Suzuki, M. Shibayama, and H. Yamazaki. "Consumption of platelets in decompression sickness of rabbits." Journal of Applied Physiology 62, no. 5 (1987): 1772–79. http://dx.doi.org/10.1152/jappl.1987.62.5.1772.

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Abstract (sommario):

Platelet behavior was studied in rabbit decompression sickness which was brought about by the exposure to 6 ATA for 40 min (bottom time) followed by rapid decompression. Platelet counts significantly decreased after the decompression. Kinetic studies with 111In-oxine-labeled platelets revealed shortened survivals of circulating platelets, and audioradiograms indicated the accumulation of radioactivity in the lungs after the decompression. Although there was no change in the mode volume of platelets after the decompression, the transient appearance of circulating smaller or fragmented platelets

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47

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

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Abstract (sommario):

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

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48

Schmaier, AH, S. Amenta, T. Xiong, GD Heda, and AM Gewirtz. "Expression of platelet C1 inhibitor." Blood 82, no. 2 (1993): 465–74. http://dx.doi.org/10.1182/blood.v82.2.465.465.

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Abstract (sommario):

Abstract Human platelets contain a pool of C1 inhibitor (C1 INH) distinct from that in plasma. Twelve normal platelet samples washed by centrifugation had a mean platelet C1 INH antigen level of 19.3 +/- 2.8 ng (mean +/- SEM) per 10(8) platelets. These values contrast with the mean +/- SEM platelet C1 INH antigen level of 6.1 +/- 0.9 per 10(8) platelets from 12 C1 INH-deficient patients. The level of platelet C1 INH correlated (r = .7) with the level of plasma C1 INH in normal individuals and patients with classic hereditary angioedema. Platelet C1 INH, like plasma C1 INH, was a 105-Kd protein

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49

Schmaier, AH, S. Amenta, T. Xiong, GD Heda, and AM Gewirtz. "Expression of platelet C1 inhibitor." Blood 82, no. 2 (1993): 465–74. http://dx.doi.org/10.1182/blood.v82.2.465.bloodjournal822465.

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Abstract (sommario):

Human platelets contain a pool of C1 inhibitor (C1 INH) distinct from that in plasma. Twelve normal platelet samples washed by centrifugation had a mean platelet C1 INH antigen level of 19.3 +/- 2.8 ng (mean +/- SEM) per 10(8) platelets. These values contrast with the mean +/- SEM platelet C1 INH antigen level of 6.1 +/- 0.9 per 10(8) platelets from 12 C1 INH-deficient patients. The level of platelet C1 INH correlated (r = .7) with the level of plasma C1 INH in normal individuals and patients with classic hereditary angioedema. Platelet C1 INH, like plasma C1 INH, was a 105-Kd protein on immun

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50

Packham, MA, MA Guccione, and KM O'Brien. "Duration of the effect of aspirin on the synthesis of thromboxane by density subpopulations of rabbit platelets stimulated with thrombin." Blood 66, no. 2 (1985): 287–90. http://dx.doi.org/10.1182/blood.v66.2.287.287.

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Abstract (sommario):

Abstract The controversy concerning the relationship between platelet buoyant density and platelet age is unresolved. Our earlier results with rabbit platelets indicate that the most-dense subpopulations are enriched in young platelets and that some platelets become less dense as they age. Other investigators have concluded that platelets either do not change in density upon aging or become more dense. In the present experiments, rabbit platelets were separated on discontinuous gradients of Stractan. Most-dense platelets synthesized significantly more thromboxane B2 (TXB2) (1.27 ng per 10(6) p

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