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Journal articles on the topic 'Vascular-platelet mechanism'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Freedman, Jane. "Toll-Like Receptors: Mechanism and Relation to Human Populations." Blood 128, no. 22 (2016): SCI—46—SCI—46. http://dx.doi.org/10.1182/blood.v128.22.sci-46.sci-46.

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Abstract Inflammation and infection are known to alter platelet count, production, and function and major studies have demonstrated that acute infection is associated with a transient 5-fold increased risk of thrombotic vascular syndromes including stroke, acute myocardial infarction, and peripheral vascular occlusion. Platelets play an intricate role in thrombosis, myocardial infarction, and thrombotic stroke and are now being appreciated for their functional innate immune receptors. More recently, platelets have been connected to the host's immune system via their ability to trap bacteria an

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2

Cohen, RA. "Platelet 5-Hydroxytryptamine and Vascular Adrenergic Nerves." Physiology 3, no. 5 (1988): 185–89. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.185.

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Platelets contain and release large amounts of 5-hydroxytryptamine that can influence the function of vascular adrenergic nerves. The immediate effect on neuronal function of low concentrations of the amine is to inhibit norepinephrine release. 5-Hydroxytryptamine may also be accumulated by the same uptake mechanism that reaccumulates norepinephrine into the adrenergic nerve endings. In diseased blood vessels where platelet aggregation occurs, 5-hydroxytryptamine may therby assume an alternative transmitter role, altering the function of the sympathetic nerves.

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Nightingale, Angus K., Philip P. James, Jayne Morris-Thurgood, et al. "Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (2001): H1334—H1339. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1334.

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Endothelial dysfunction reflects reduced nitric oxide (NO) bioavailability due to either reduced production, inactivation of NO, or reduced smooth muscle responsiveness. Oral methionine loading causes acute endothelial dysfunction in healthy subjects and provides a model in which to study mechanisms. Endothelial function was assessed using flow-mediated dilatation (FMD) of the brachial artery in humans. Three markers of oxidative stress were measured ex vivo in venous blood. NO responsiveness was assessed in vascular smooth muscle and platelets. Oral methionine loading induced endothelial dysf

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4

Nesbitt, Warwick S., Simon Giuliano, Suhasini Kulkarni, Sacha M. Dopheide, Ian S. Harper, and Shaun P. Jackson. "Intercellular calcium communication regulates platelet aggregation and thrombus growth." Journal of Cell Biology 160, no. 7 (2003): 1151–61. http://dx.doi.org/10.1083/jcb.200207119.

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The ability of platelets to form stable adhesion contacts with other activated platelets (platelet cohesion or aggregation) at sites of vascular injury is essential for hemostasis and thrombosis. In this study, we have examined the mechanisms regulating cytosolic calcium flux during the development of platelet–platelet adhesion contacts under the influence of flow. An examination of platelet calcium flux during platelet aggregate formation in vitro demonstrated a key role for intercellular calcium communication (ICC) in regulating the recruitment of translocating platelets into developing aggr

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5

Mezger, M., K. Göbel, P. Kraft, S. G. Meuth, C. Kleinschnitz, and H. F. Langer. "Platelets and vascular inflammation of the brain." Hämostaseologie 35, no. 03 (2015): 244–51. http://dx.doi.org/10.5482/hamo-14-11-0071.

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SummaryThere is emerging evidence that platelets have an important role in inflammation beyond their involvement in hemostasis. Platelets can contribute to inflammatory reactions via crosstalk both with immune cells and endothelial cells. Inflamed vessels are characterized by the presence of activated endothelial cells. These activated endothelial cells upregulate receptors necessary for leukocyte recruitment, but also for the adhesion of platelets. Subsequently, immune cells can bind to platelets through adhesion receptors presented on the platelet surface, thus supporting leukocyte recruitme

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6

Gong, Shengyang, and Zheng Cao. "Research Progress on the Anti-Atherosclerotic Effect and Mechanism of Tetramethylpyrazine." Journal of Clinical and Nursing Research 8, no. 6 (2024): 94–99. http://dx.doi.org/10.26689/jcnr.v8i6.7032.

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Atherosclerosis is a chronic vascular disease and the most common pathological change of cardiovascular disease. Its pathogenesis is closely related to inflammation, oxidative stress, lipid accumulation, and calcinosis. Tetramethylpyrazine plays an anti-atherosclerotic role by regulating lipid metabolism, inhibiting foam cell formation, alleviating inflammation, inhibiting vascular calcification and abnormal platelet activation, and has a cardiovascular protective effect. Therefore, this paper summarized the research progress of the anti-atherosclerosis effect and mechanism of tetramethylpyraz

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Meng, Qingyu, Xichun Li, Mingyu Zhao, Shusen Lin, Xiangwen Yu та Guanglong Dong. "Study on the Mechanism of Platelet-Released Clusterins Inducing Restenosis after Carotid Endarterectomy by Activating TLR3/NF-κb p65 Signaling Pathway". Journal of Healthcare Engineering 2022 (10 січня 2022): 1–8. http://dx.doi.org/10.1155/2022/7631126.

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This study aimed to explore the role of clusterin released by platelet aggregation in restenosis after carotid endarterectomy. 35 patients who underwent carotid endarterectomy due to carotid artery stenosis were enrolled in this study. They were admitted to the Third Affiliated Hospital of Qiqihar Medical University from January 2018 to January 2019. All the patients were divided into two groups: the restenosis group and the nonrestenosis group, according to the follow-up results within 12 months. Peripheral blood was collected on the first day, 6 months, and 12 months after operation. The exp

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8

Gavrilovskaya, Irina N., Elena E. Gorbunova, and Erich R. Mackow. "Pathogenic Hantaviruses Direct the Adherence of Quiescent Platelets to Infected Endothelial Cells." Journal of Virology 84, no. 9 (2010): 4832–39. http://dx.doi.org/10.1128/jvi.02405-09.

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ABSTRACT Hantavirus infections are noted for their ability to infect endothelial cells, cause acute thrombocytopenia, and trigger 2 vascular-permeability-based diseases. However, hantavirus infections are not lytic, and the mechanisms by which hantaviruses cause capillary permeability and thrombocytopenia are only partially understood. The role of β3 integrins in hemostasis and the inactivation of β3 integrin receptors by pathogenic hantaviruses suggest the involvement of hantaviruses in altered platelet and endothelial cell functions that regulate permeability. Here, we determined that pathog

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9

Mousa, Shaker, and Joel Bennett. "Platelet Function Inhibitors in the Year 2000." Thrombosis and Haemostasis 85, no. 03 (2001): 395–400. http://dx.doi.org/10.1055/s-0037-1615595.

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SummaryPlatelet thrombi are responsible for much of the morbidity and mortality of arterial vascular disease (1). Because platelet inhibitors such as aspirin have proven to be of benefit to patients with these disorders, there has been a directed search for more potent anti-platelet agents. The following discussion addresses the mechanism of action and clinical utility of the currently available platelet function inhibitors. Although in theory these agents could impair platelet adhesion, aggregation, secretion, or platelet procoagulant activity, in practice they are focused almost exclusively

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10

Markmeyer, Paulina, Franziska Lochmann, Kunal Kumar Singh, et al. "Procoagulant Extracellular Vesicles Alter Trophoblast Differentiation in Mice by a Thrombo-Inflammatory Mechanism." International Journal of Molecular Sciences 22, no. 18 (2021): 9873. http://dx.doi.org/10.3390/ijms22189873.

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Procoagulant extracellular vesicles (EV) and platelet activation have been associated with gestational vascular complications. EV-induced platelet-mediated placental inflammasome activation has been shown to cause preeclampsia-like symptoms in mice. However, the effect of EV-mediated placental thrombo-inflammation on trophoblast differentiation remains unknown. Here, we identify that the EV-induced thrombo-inflammatory pathway modulates trophoblast morphology and differentiation. EVs and platelets reduce syncytiotrophoblast differentiation while increasing giant trophoblast and spongiotrophobl

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11

Lee, Bo Kyung, Hye Jin Jee та Yi-Sook Jung. "Aβ1–40-Induced Platelet Adhesion Is Ameliorated by Rosmarinic Acid through Inhibition of NADPH Oxidase/PKC-δ/Integrin αIIbβ3 Signaling". Antioxidants 10, № 11 (2021): 1671. http://dx.doi.org/10.3390/antiox10111671.

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In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer’s disease (AD). Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however, the underlying mechanism remains elusive. In the present study, we aimed to elucidate the signaling pathway of platelet adhesion induced by Aβ1–40, the major form of circulating Aβ, through Western blotting, immunofluorescence confocal microscopy, and fluorescence-activated cell sorting analysis. Additi

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Curcio, Francesco, Isabella Pegoraro, Patrizia Dello Russo, Edmondo Falleti, Giusepplna Perrella, and Antonio Ceriello. "Sod and GSH Inhibit the High Glucose-Induced Oxidative Damage and the PDGF Increased Secretion in Cultured Human Endothelial Cells." Thrombosis and Haemostasis 74, no. 03 (1995): 969–73. http://dx.doi.org/10.1055/s-0038-1649857.

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SummaryPoor control of blood glucose has been established as a key pathogenetic mechanism in the vascular complications of diabetes. It has been reported that glucose may autooxidize generating free radicals which have been suggested to delay proliferation, to modify mobility, to influence platelet-derived growth factor and other secretory protein production in a variety of cell systems. Platelet-derived growth factor, in turn, may induce proliferation and migration of vascular smooth muscle cells and thus play a role in atherogenesis. In the present study the effects of antioxidants on the hi

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Evangelista, Virgilio, Giovanni de Gaetano та Chiara Cerletti. "P-Selectin-β2-Integrin Cross-Talk: A Molecular Mechanism For Polymorphonuclear Leukocyte Recruitment At The Site Of Vascular Damage". Thrombosis and Haemostasis 82, № 08 (1999): 787–93. http://dx.doi.org/10.1055/s-0037-1615912.

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IntroductionPlatelets activated at the site of vascular damage play a pivotal role in polymorphonuclear (PMN) leukocyte accumulation in a growing thrombus2,3 and may substitute endothelial cells in the recruitment and migration of leukocytes through damaged vessel wall.4 Leukocytes, accumulated in a platelet thrombus, can contribute to further platelet activation5 and to increased fibrin deposition.6 These events, on the one hand, may contribute to the maintenance of vascular and tissue integrity. They may, however, play a pathogenic role in inflammatory and thrombotic disease, providing some

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14

Kirsch, Carl M., James J. Brokaw, Debra M. Prow, and Gary W. White. "Mechanism of Platelet Activating Factor-Induced Vascular Leakage in the Rat Trachea." Experimental Lung Research 18, no. 4 (1992): 447–59. http://dx.doi.org/10.3109/01902149209064339.

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15

Annarapu, Gowtham K., Stefanie Taiclet, Scott Hahn, et al. "Obesity-Induced Platelet Mitofusin-1 Expression Causes Vascular Dysfunction." Blood 142, Supplement 1 (2023): 2571. http://dx.doi.org/10.1182/blood-2023-187693.

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Background:The growing epidemic of obesity is strongly linked to cardiovascular disease (CVD). Obesity leads to endothelial dysfunction, an instigating event that drives vascular injury and subsequent CVD, but the mechanisms by which obesity causes endothelial dysfunction remain unclear. Platelets circulate proximal to the endothelium and are traditionally thought to contribute to obesity-associated vasculopathy through thrombotic activation. However, platelets are metabolically active and release vaso-modulatory molecules into their environment and the role of these functions have not been ex

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16

Bertozzi, Cara C., Alec A. Schmaier, Patricia Mericko, et al. "Platelets regulate lymphatic vascular development through CLEC-2–SLP-76 signaling." Blood 116, no. 4 (2010): 661–70. http://dx.doi.org/10.1182/blood-2010-02-270876.

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Abstract Although platelets appear by embryonic day 10.5 in the developing mouse, an embryonic role for these cells has not been identified. The SYK–SLP-76 signaling pathway is required in blood cells to regulate embryonic blood-lymphatic vascular separation, but the cell type and molecular mechanism underlying this regulatory pathway are not known. In the present study we demonstrate that platelets regulate lymphatic vascular development by directly interacting with lymphatic endothelial cells through C-type lectin-like receptor 2 (CLEC-2) receptors. PODOPLANIN (PDPN), a transmembrane protein

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17

Stellos, Konstantinos, Victoria Panagiota, Andreas Kögel, Thomas Leyhe, Meinrad Gawaz, and Christoph Laske. "Predictive Value of Platelet Activation for the Rate of Cognitive Decline in Alzheimer's Disease Patients." Journal of Cerebral Blood Flow & Metabolism 30, no. 11 (2010): 1817–20. http://dx.doi.org/10.1038/jcbfm.2010.140.

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Vascular risk factors contribute to the progression of dementia in Alzheimer's disease (AD) and influence platelet activation. However, the degree of platelet activation as a possible underlying mechanism of this progression has not been studied till now. Significantly higher baseline expression of both platelet activation biomarkers, activated glycoprotein IIb–IIIa complex and P-selectin, was observed in patients with AD with fast cognitive decline compared with AD patients with slow cognitive decline during a 1-year follow-up period. These results suggest that platelet activation could be a

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18

Durante, W., VB Schini, MH Kroll, et al. "Platelets inhibit the induction of nitric oxide synthesis by interleukin-1 beta in vascular smooth muscle cells." Blood 83, no. 7 (1994): 1831–38. http://dx.doi.org/10.1182/blood.v83.7.1831.1831.

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Abstract We have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1 beta (IL- 1 beta)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1 beta resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels. The releasate from collagen-aggregated plate

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Durante, W., VB Schini, MH Kroll, et al. "Platelets inhibit the induction of nitric oxide synthesis by interleukin-1 beta in vascular smooth muscle cells." Blood 83, no. 7 (1994): 1831–38. http://dx.doi.org/10.1182/blood.v83.7.1831.bloodjournal8371831.

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We have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1 beta (IL- 1 beta)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1 beta resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels. The releasate from collagen-aggregated platelets bloc

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Walsh, G. M., J. J. Mermod, A. Hartnell, A. B. Kay, and A. J. Wardlaw. "Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is alpha 4 beta 1 (very late antigen-4) dependent." Journal of Immunology 146, no. 10 (1991): 3419–23. http://dx.doi.org/10.4049/jimmunol.146.10.3419.

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Abstract Eosinophils, through their ability to generate an array of potent mediators, are thought to be the major effector cells in a number of conditions, including parasitic infection, asthma, and other allergic diseases. The mechanism(s) by which eosinophils, as opposed to neutrophils, accumulate at inflammatory sites is unknown. One possible mechanism would be an eosinophil-specific pathway of adhesion to vascular endothelium. In this study we have demonstrated that human eosinophils, but not neutrophils, constitutively express alpha 4 beta 1 (CD49d/CD29). Expression was not increased on l

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Prokurat, Monika, Katarzyna Grudnik, Wojciech Niemczyk, et al. "Platelet-Rich Plasma - a remedy present in every human being. History, functioning, and the benefits of therapy using it." Polski Merkuriusz Lekarski 52, no. 2 (2024): 240–45. http://dx.doi.org/10.36740/merkur202402114.

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Platelet-rich plasma is an autologous product used in restorative medicine. It contains a high concentration of platelets, which are rich in growth factors and other biologically active substances known for their ability to stimulate regenerative processes in the body. Currently, research is being conducted into the use of platelet-rich plasma in many areas of medicine. This publication provides information on the nature, mechanism of action, therapeutic properties and application of autologous platelet-rich plasma in medicine. Furthermore, ongoing investigations explore its potential in wound

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Doll, D. C., Q. S. Ringenberg, and J. W. Yarbro. "Vascular toxicity associated with antineoplastic agents." Journal of Clinical Oncology 4, no. 9 (1986): 1405–17. http://dx.doi.org/10.1200/jco.1986.4.9.1405.

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Vascular complications associated with antineoplastic agents are being reported with increasing frequency. Such vascular toxicity is clinically heterogeneous, ranging from asymptomatic arterial lesions to a fatal thrombotic microangiopathic syndrome. Mitomycin is most commonly implicated in the thrombotic microangiopathic syndrome, while bleomycin, either alone or in combination with a vinca alkaloid or cisplatin, appears to be an important cause of Raynaud's phenomenon. Acute arterial ischemic events, ie, myocardial infarction and cerebrovascular accidents, occur most frequently after cisplat

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Cho, Jaehyung, Daniel R. Kennedy, Lin Lin та ін. "Protein disulfide isomerase capture during thrombus formation in vivo depends on the presence of β3 integrins". Blood 120, № 3 (2012): 647–55. http://dx.doi.org/10.1182/blood-2011-08-372532.

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Abstract Extracellular protein disulfide isomerase (PDI) is required for platelet thrombus formation and fibrin generation after arteriolar wall injury in live mice. PDI is secreted from platelets and endothelial cells on cellular activation, but the mechanism of capture of secreted PDI within the injured vasculature is unknown. We establish that, like the endothelial β3 integrin αVβ3, the platelet integrin αIIbβ3 binds PDI. PDI also binds to recombinant β3. Using intravital microscopy, we demonstrate that PDI accumulation at the site of laser-induced arteriolar wall injury is markedly reduced

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Ball, Stephen G., C. Adrian Shuttleworth, and Cay M. Kielty. "Vascular endothelial growth factor can signal through platelet-derived growth factor receptors." Journal of Cell Biology 177, no. 3 (2007): 489–500. http://dx.doi.org/10.1083/jcb.200608093.

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Vascular endothelial growth factor (VEGF-A) is a crucial stimulator of vascular cell migration and proliferation. Using bone marrow–derived human adult mesenchymal stem cells (MSCs) that did not express VEGF receptors, we provide evidence that VEGF-A can stimulate platelet-derived growth factor receptors (PDGFRs), thereby regulating MSC migration and proliferation. VEGF-A binds to both PDGFRα and PDGFRβ and induces tyrosine phosphorylation that, when inhibited, results in attenuation of VEGF-A–induced MSC migration and proliferation. This mechanism was also shown to mediate human dermal fibrob

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Villagra, Jose D., James T. Nichols, Mark T. Gladwin, and Gregory J. Kato. "Platelets from Patients with Sickle Cell Disease and Pulmonary Arterial Hypertension Are Hypersensitive to Agonist-Induced Activation." Blood 108, no. 11 (2006): 1239. http://dx.doi.org/10.1182/blood.v108.11.1239.1239.

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Abstract Pulmonary arterial hypertension (PAH) in sickle cell disease (SCD) is associated with chronic hemolysis and nitric oxide (NO) consumption and characterized by abnormal vascular tone, vascular proliferation and thrombosis. In previous studies, we demonstrated that increased platelet activation is linked to the severity of PAH in SCD. In addition, we reported that patients with SCD and secondary PAH have decreased platelet activation when given sildenafil, a finding that highlights the role of nitric oxide inhibition by hemolysis in this pathological mechanism. Since the vascular homeos

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Zhu, Ying, Dan Shu, Xue Gong та ін. "Platelet-Derived TGF (Transforming Growth Factor)-β1 Enhances the Aerobic Glycolysis of Pulmonary Arterial Smooth Muscle Cells by PKM2 (Pyruvate Kinase Muscle Isoform 2) Upregulation". Hypertension 79, № 5 (2022): 932–45. http://dx.doi.org/10.1161/hypertensionaha.121.18684.

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Background: Metabolic reprogramming is a hallmark of pulmonary arterial hypertension. Platelet activation has been implicated in pulmonary arterial hypertension (PAH), whereas the role of platelet in the pathogenesis of PAH remains unclear. Methods: First, we explored the platelet function of semaxanib‚ a inhibitor of VEGF receptor (SU5416)/hypoxia mice and monocrotaline-injected rats PAH model. Then we investigated pulmonary arterial smooth muscle cell aerobic glycolysis after being treated with platelet supernatant. TGF (transforming growth factor)-βRI, pyruvate kinase muscle 2, and other an

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Karhausen, Jörn, Hae Woong Choi, Krishna Rao Maddipati, et al. "Platelets trigger perivascular mast cell degranulation to cause inflammatory responses and tissue injury." Science Advances 6, no. 12 (2020): eaay6314. http://dx.doi.org/10.1126/sciadv.aay6314.

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Platelet responses have been associated with end-organ injury and mortality following complex insults such as cardiac surgery, but how platelets contribute to these pathologies remains unclear. Our studies originated from the observation of microvascular platelet retention in a rat cardiac surgery model. Ensuing work supported the proximity of platelet aggregates with perivascular mast cells (MCs) and demonstrated that platelet activation triggered systemic MC activation. We then identified platelet activating factor (PAF) as the platelet-derived mediator stimulating MCs and, using chimeric an

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Korbut, R., A. Dembińska-Kieć, J. Świȩs, A. Źmuda, and R. J. Gryglewski. "On the Mechanism of Thrombolytic Action of Thromboxane Synthetase Inhibitors." Thrombosis and Haemostasis 58, no. 03 (1987): 827–30. http://dx.doi.org/10.1055/s-0038-1645998.

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SummaryUsing our in vivo model for studying drugs which prevent deposition of thrombi or dissipate thrombi formed in extracorporeal circulation over a collagen strip superfused with arterial blood of anaesthetized and heparinized cats, we have found that dazoxiben - a thromboxane synthetase inhibitor - possesses not only antithrombotic but also thrombolytic potency in vivo (ED50 = 3.8 mg/kg i.v.). The thrombolytic potency of dazoxiben was antagonized by aspirin at a dose of 50 mg/kg i.v. Moreover, dazoxiben stimulated the generation of prostacyclin in isolated rat aortic slices incubated in pl

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Ruggeri, Z. M. "Platelet and von Willebrand factor interactions at the vessel wall." Hämostaseologie 24, no. 01 (2004): 1–11. http://dx.doi.org/10.1055/s-0037-1619601.

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SummaryThe process of platelet thrombus formation contributes to the haemostatic response that prevents excessive blood loss after tissue injury, but may become a life-threatening disease mechanism by causing the acute thrombotic occlusion of atherosclerotic arteries. The participation of platelets in the formation of thrombi is centered on their adhesive properties and the ability to respond to stimuli with rapid activation. Platelet adhesion and activation are multifaceted and modulated by different environmental conditions, suggesting that it should be possible to obtain a selective pharmac

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Horton, Lucy Elise, Brian Sullivan, Robert F. Garry, Donald S. Grant, and Michael B. Oldstone. "Endothelial dysfunction in the pathogenesis of acute Lassa Fever." Journal of Immunology 200, no. 1_Supplement (2018): 126.22. http://dx.doi.org/10.4049/jimmunol.200.supp.126.22.

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Abstract Lassa fever (LF) is an acute disease characterized by enhanced vascular permeability resulting from infection with Lassa virus (LV), a non-lytic, Old World arenavirus. Animal models of arenavirus-induced vascular damage suggest that cytotoxic CD8+ T cells serve a critical role in the destruction of vascular endothelium by destroying LV infected endothelial cells as well as impairing platelet aggregation. Using plasma samples from acute LF patients, we sought to identify predictive biomarkers associated with endothelial integrity and platelet aggregation in fatal versus non-fatal LF ca

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Bozzi, Valeria, Emanuele Panza, Serena Barozzi, et al. "Mutations responsible for MYH9-related thrombocytopenia impair SDF-1-driven migration of megakaryoblastic cells." Thrombosis and Haemostasis 106, no. 10 (2011): 693–704. http://dx.doi.org/10.1160/th11-02-0126.

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SummaryMYH9-related disease (MYH9-RD) is an autosomal-dominant thrombocytopenia caused by mutations in the gene for the heavy chain of nonmuscle myosin-IIA (NMMHC-IIA). Recent in vitro studies led to the hypothesis that thrombocytopenia of MYH9-RD derives from an ectopic platelet release by megakaryocytes in the osteoblastic areas of bone marrow (BM), which are enriched in type I collagen, rather than in vascular spaces. SDF-1-driven migration of megakaryocytes within BM to reach the vascular spaces is a key mechanism for platelet biogenesis. Since myosin-IIA is implicated in polarised migrati

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Yan, Yi, Yang-Yang He, Xin Jiang, et al. "DNA methyltransferase 3B deficiency unveils a new pathological mechanism of pulmonary hypertension." Science Advances 6, no. 50 (2020): eaba2470. http://dx.doi.org/10.1126/sciadv.aba2470.

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DNA methylation plays critical roles in vascular pathology of pulmonary hypertension (PH). The underlying mechanism, however, remains undetermined. Here, we demonstrate that global DNA methylation was elevated in the lungs of PH rat models after monocrotaline administration or hypobaric hypoxia exposure. We showed that DNA methyltransferase 3B (DNMT3B) was up-regulated in both PH patients and rodent models. Furthermore, Dnmt3b−/− rats exhibited more severe pulmonary vascular remodeling. Consistently, inhibition of DNMT3B promoted proliferation/migration of pulmonary artery smooth muscle cells

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Lev, Eli, Zeev Estrov, Khatira Aboulfatova, et al. "Potential role of activated platelets in homing of human endothelial progenitor cells to subendothelial matrix." Thrombosis and Haemostasis 96, no. 10 (2006): 498–504. http://dx.doi.org/10.1160/th06-05-0250.

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SummaryEndothelial progenitor cells (EPCs) mobilize from the bone marrow in response to tissue injury and participate in vascular repair. However, there is limited data about the homing mechanisms of EPCs to vascular injury sites. Recently animal experiments indicated that platelets playa role in recruitment of EPCs to injury sites. However, data on the possible interaction between platelets and EPCs within the human system are limited. We, therefore, examined in-vitro human platelet-EPC interaction under static and flow conditions. Human EPCs were isolated from donated buffy coats by magnetic

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Baugh, Robert F. "Platelets and whole blood coagulation." Perfusion 15, no. 1 (2000): 41–50. http://dx.doi.org/10.1177/026765910001500107.

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In our early work in developing activated clotting time (ACT) assays, it became apparent that changes occurred in coagulation times as a whole blood sample aged (0-6 h). Subsequent studies showed that the coagulation parameters of plasma obtained from the samples remained stable during this time frame. These changes in whole blood clotting times during storage were eventually traced to the platelets. Several years of work demonstrated that this change was due to the removal of the blood from the vascular lining. This recalled a mechanism that was originally put forth in the 1970s with the disc

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Belyaev, Aleksey V. "Computer modelling of initial platelet adhesion during microvascular thrombosis." Russian Journal of Numerical Analysis and Mathematical Modelling 34, no. 5 (2019): 241–51. http://dx.doi.org/10.1515/rnam-2019-0020.

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Abstract Hemostasis is one of the most important protective mechanisms that functions to maintain vascular integrity and prevent bleeding. In arterial and microvascular circulation, where the near-wall shear stress is relatively high, the hemostatic response begins with aggregation of platelets on the injured endothelium or collagen. Regulation of hemostasis and thrombosis is immensely complex, as it depends on the blood cell adhesion and fluid dynamics. A possible regulatory mechanism relies on the coil-stretch transitions in a plasma protein — von Willebrand factor — that serves as a ligand

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Bombeli, Thomas, Barbara R. Schwartz та John M. Harlan. "Adhesion of Activated Platelets to Endothelial Cells: Evidence for a GPIIbIIIa-dependent Bridging Mechanism and Novel Roles for Endothelial Intercellular Adhesion Molecule 1 (ICAM-1), αvβ3 Integrin, and GPIbα". Journal of Experimental Medicine 187, № 3 (1998): 329–39. http://dx.doi.org/10.1084/jem.187.3.329.

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Although it has been reported that activated platelets can adhere to intact endothelium, the receptors involved have not been fully characterized. Also, it is not clear whether activated platelets bind primarily to matrix proteins at sites of endothelial cell denudation or directly to endothelial cells. Thus, this study was designed to further clarify the mechanisms of activated platelet adhesion to endothelium. Unstimulated human umbilical vein endothelial cell (HUVEC) monolayers were incubated with washed, stained, and thrombin-activated human platelets. To exclude matrix involvement, HUVEC

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Arumugam, Vidhyalakshmi, Jianzhong An, Michelle Bordas, and Rashmi Sood. "An Experimental Model of Platelet Activation at the Feto-Maternal Interface." Blood 124, no. 21 (2014): 2766. http://dx.doi.org/10.1182/blood.v124.21.2766.2766.

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Abstract Background and Objectives: A developing fetus relies on the placenta for nutrition and other essential functions. To perform these functions human and rodent placenta forms unusual vascular spaces filled with maternal blood and directly accessible to specialized placental cells, called trophoblast cells. Such vascular spaces are not found anywhere else in the body. Trophoblast cells are of zygotic origin and they express a repertoire of molecules with anticoagulant and anti-platelet activities (PMID 16380449). In addition, they constitutively express Tissue Factor. Given these peculia

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Kovalenko, T. A., and M. A. Panteleev. "Membrane-dependent reactions of blood coagulation: classical view and state-of-the-art concepts." Biologičeskie membrany 41, no. 5-6 (2024): 427–47. http://dx.doi.org/10.31857/s0233475524050063.

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The complex mechanism called hemostasis evolved in living organisms to prevent blood loss when a blood vessel is damaged. In this process, two closely interconnected systems are distinguished: platelet-vascular and plasmatic hemostasis. Plasmatic hemostasis is a system of proteolytic reactions, in which blood plasma proteins called coagulation factors are involved. A key feature of this system is the localization of enzymatic reactions on the surface of phospholipid membranes, which increases their rate by up to 5 orders of magnitude. This review describes the basic mechanisms of coagulation f

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Spinelli, S. L., J. J. O'Brien, S. Bancos, et al. "The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects." PPAR Research 2008 (2008): 1–16. http://dx.doi.org/10.1155/2008/328172.

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Historically, platelets were viewed as simple anucleate cells responsible for initiating thrombosis and maintaining hemostasis, but clearly they are also key mediators of inflammation and immune cell activation. An emerging body of evidence links platelet function and thrombosis to vascular inflammation. peroxisome proliferator-activated receptors (PPARs) play a major role in modulating inflammation and, interestingly, PPARs (PPARβ/δand PPARγ) were recently identified in platelets. Additionally, PPAR agonists attenuate platelet activation; an important discovery for two reasons. First, activat

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Ding, Yonghui, Zhilu Yang, Cathy W. C. Bi, et al. "Modulation of protein adsorption, vascular cell selectivity and platelet adhesion by mussel-inspired surface functionalization." J. Mater. Chem. B 2, no. 24 (2014): 3819–29. http://dx.doi.org/10.1039/c4tb00386a.

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Terada, Lance S., Brooks M. Hybertson, Kevin G. Connelly, David Weill, Dale Piermattei, and John E. Repine. "XO increases neutrophil adherence to endothelial cells by a dual ICAM-1 and P-selectin-mediated mechanism." Journal of Applied Physiology 82, no. 3 (1997): 866–73. http://dx.doi.org/10.1152/jappl.1997.82.3.866.

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Terada, Lance S., Brooks M. Hybertson, Kevin G. Connelly, David Weill, Dale Piermattei, and John E. Repine. XO increases neutrophil adherence to endothelial cells by a dual ICAM-1 and P-selectin-mediated mechanism. J. Appl. Physiol. 82(3): 866–873, 1997.—Circulating xanthine oxidase (XO) can modify adhesive interactions between neutrophils and the vascular endothelium, although the mechanisms underlying this effect are not clear. We found that treatment with XO of bovine pulmonary artery endothelial cells (EC), but not neutrophils or plasma, increased adherence, suggesting that XO had its prim

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Jin, Panshi, Qiao Pan, Yize Lin, et al. "Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells." Oxidative Medicine and Cellular Longevity 2023 (February 20, 2023): 1–23. http://dx.doi.org/10.1155/2023/2345279.

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As a critical member in wound healing, vascular endothelial cells (ECs) impaired under high levels of reactive oxygen species (ROS) would hamper neovascularization. Mitochondria transfer can reduce intracellular ROS damage under pathological condition. Meanwhile, platelets can release mitochondria and alleviate oxidative stress. However, the mechanism by which platelets promote cell survival and reduce oxidative stress damage has not been clarified. Here, first, we selected ultrasound as the best method for subsequent experiments by detecting the growth factors and mitochondria released from m

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Godyna, S., M. Diaz-Ricart, and WS Argraves. "Fibulin-1 mediates platelet adhesion via a bridge of fibrinogen." Blood 88, no. 7 (1996): 2569–77. http://dx.doi.org/10.1182/blood.v88.7.2569.bloodjournal8872569.

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Fibulin-1 is a component of the extracellular matrix that surrounds vascular smooth muscle. This observation, along with the recent finding that fibulin-1 can bind fibrinogen (J Biol Chem 270:19458, 1995), prompted investigation into the potential role of fibulin-1 as a thrombogenic agent. In perfusion chamber assays, platelets in whole blood under flow conditions attached and spread on surfaces coated with fibulin-1. This adhesion was completely blocked by fibulin-1 antibodies. Platelets free of plasma did not attach to fibulin-1 coated surfaces; however, with the addition of fibrinogen, plat

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Möller, Kerstin, Oliver Adolph, Jennifer Grünow, et al. "Mechanism and functional impact of CD40 ligand-induced von Willebrand factor release from endothelial cells." Thrombosis and Haemostasis 113, no. 05 (2015): 1095–108. http://dx.doi.org/10.1160/th14-04-0336.

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SummaryCo-stimulation via CD154 binding to CD40, pivotal for both innate and adaptive immunity, may also link haemostasis to vascular remodelling. Here we demonstrate that human platelet-bound or recombinant soluble CD154 (sCD154) elicit the release from and tethering of ultra-large (UL) von Willebrand factor (vWF) multimers to the surface of human cultured endothelial cells (ECs) exposed to shear stress. This CD40-mediated ULVWF multimer release from the Weibel-Palade bodies was triggered by consecutive activation of TRAF6, the tyrosine kinase c-Src and phospholipase Cγ1 followed by inositol-

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Kirchhofer, Daniel, Markus A. Riederer, and Hans R. Baumgartner. "Specific Accumulation of Circulating Monocytes and Polymorphonuclear Leukocytes on Platelet Thrombi in a Vascular Injury Model." Blood 89, no. 4 (1997): 1270–78. http://dx.doi.org/10.1182/blood.v89.4.1270.

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AbstractThe adhesion of leukocytes to platelets deposited at the site of vascular injury may represent an important mechanism by which leukocytes contribute to hemostasis and thrombosis. In this study, we examined whether, in comparison with their distribution in circulating blood, certain leukocyte types are enriched at sites of platelet deposition. We used an experimental vascular injury model, in which human fibrillar collagen was exposed to anticoagulated human whole blood flowing through parallel-plate chambers (venous shear rate, 65/s). The platelet-adherent leukocytes were detached by E

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Laurindo, F. R., R. E. Goldstein, N. J. Davenport, D. Ezra, and G. Z. Feuerstein. "Mechanisms of hypotension produced by platelet-activating factor." Journal of Applied Physiology 66, no. 6 (1989): 2681–90. http://dx.doi.org/10.1152/jappl.1989.66.6.2681.

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Platelet-activating factor (PAF) is a phospholipid mediator that induces cardiovascular collapse and release of the secondary mediator thromboxane A2 (TxA2). To clarify mechanisms involved in this collapse and, specifically, the relative contribution of left ventricular and right ventricular dysfunction, we studied 12 open-chest pigs. PAF infusion (0.04–0.28 nmol.kg-1.min-1) induced a 5- to 120-fold increase in pulmonary vascular resistance, a 75–98% fall in cardiac output, and systemic arterial hypotension. Right ventricular failure was indicated by chamber enlargement, decreased shortening,

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Hildemann, Steven, Christian Schulz, Daniela Fraccarollo, et al. "Fractalkine promotes platelet activation and vascular dysfunction in congestive heart failure." Thrombosis and Haemostasis 111, no. 04 (2014): 725–35. http://dx.doi.org/10.1160/th13-08-0640.

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SummaryEndothelial dysfunction and enhanced platelet reactivity in congestive heart failure (CHF) contribute to poor prognosis. CHF patients display an impaired responsiveness to clopidogrel. Fractalkine activates platelets and elevated plasma levels of this chemokine are a feature of CHF. We here addressed the interrelation of fractalkine, platelet reactivity and clopidogrel efficacy in humans and rats with CHF. Fractalkine serum levels determined by ELISA were increased in CHF patients (CHF: 1548 ± 650 pg/ml; Control: 968 ± 575 pg/ml, p<0.01) and following CHF induction in rats (CHF: 1509

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McCall, T. B., N. K. Boughton-Smith, R. M. J. Palmer, B. J. R. Whittle, and S. Moncada. "Synthesis of nitric oxide from l-arginine by neutrophils. Release and interaction with superoxide anion." Biochemical Journal 261, no. 1 (1989): 293–96. http://dx.doi.org/10.1042/bj2610293.

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Stimulated rat peritoneal neutrophils release a platelet inhibitory factor with the pharmacological properties of NO. This release is inhibited by NG-monomethyl-L-arginine and L-canavanine, indicating that it occurs through a mechanism similar to that in vascular endothelial cells and macrophages. As the degree of stimulation increases, the factor released is progressively inactivated by concomitant release of superoxide anions.

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Roberts, Wayne, Simbarashe Magwenzi, Ahmed Aburima, and Khalid M. Naseem. "Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade." Blood 116, no. 20 (2010): 4297–306. http://dx.doi.org/10.1182/blood-2010-01-265561.

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Abstract Cyclic adenosine monophosphate (cAMP)-dependent signaling modulates platelet function at sites of vascular injury. Here we show that thrombospondin-1 (TSP-1) prevents cAMP/protein kinase A (PKA) signaling through a CD36-dependent mechanism. Prostaglandin E1 (PGE1) induced a robust inhibition of both platelet aggregation and platelet arrest under physiologic conditions of flow. Exogenous TSP-1 reduced significantly PGE1-mediated inhibition of both platelet aggregation and platelet arrest. TSP-1 prevented PGE1-stimulated cAMP accrual and phosphorylation of PKA substrates, through a mech

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Haguet, Hélène, Jonathan Douxfils, Christian Chatelain, Carlos Graux, François Mullier, and Jean-Michel Dogné. "BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?" TH Open 02, no. 01 (2018): e68-e88. http://dx.doi.org/10.1055/s-0038-1624566.

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AbstractImatinib, the first-in-class BCR-ABL tyrosine kinase inhibitor (TKI), had been a revolution for the treatment of chronic myeloid leukemia (CML) and had greatly enhanced patient survival. Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective. However, these treatments have been associated with arterial occlusive events. This review gathers clinical data and experiments about the pathophysiology of these arterial occlusive events with BCR-ABL TKIs. Imatinib is associ

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