Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release

Rinder, CS; Student, LA; Bonan, JL; Rinder, HM; Smith, Bernard

doi:10.1182/blood.v82.2.505.505

Cited by 114 publications

(3 citation statements)

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“…It is important to note here that this increased delivery and penetration observed with clopidogrel may not necessarily extend to other anti-platelet drugs. For example, aspirin may not show this effect due to a lack of suppression of platelet granule secretion [20].…”

Section: Discussionmentioning

confidence: 99%

Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery

Pandey¹,

Sarangi²,

Chien³

et al. 2014

Nanotechnology

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Tumor vasculature is critically dependent on platelet mediated hemostasis and disruption of the same can augment delivery of nano-formulation based chemotherapeutic agents which depend on enhanced permeability and retention for tumor penetration. Here, we evaluated the role of Clopidogrel, a well-known inhibitor of platelet aggregation, in potentiating the tumor cytotoxicity of cisplatin nano-formulation in a murine breast cancer model. In vivo studies in murine syngeneic 4T1 breast cancer model showed a significant greater penetration of macromolecular fluorescent nanoparticles after clopidogrel pretreatment. Compared to self-assembling cisplatin nanoparticles (SACNs), combination therapy with clopidogrel and SACN was associated with a 4 fold greater delivery of cisplatin to tumor tissue and a greater reduction in tumor growth as well as higher survival rate. Clopidogrel enhances therapeutic efficiency of novel cisplatin based nano-formulations agents by increasing tumor drug delivery and can be used as a potential targeting agent for novel nano-formulation based chemotherapeutics.

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Section: Discussionmentioning

confidence: 99%

Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery

Pandey¹,

Sarangi²,

Chien³

et al. 2014

Nanotechnology

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“…58 This pathway is not essential for GPIIb/IIIa activation, secretion, and aggregation. 59 Therefore, blocking this Fig. 5 G-protein coupled seven-transmembrane receptor signaling in platelets.…”

Section: Signal Transduction-stimulatory Signalingmentioning

confidence: 99%

“…58 This pathway is not essential for GPIIb/IIIa activation, secretion, and aggregation. 59 Therefore, blocking this pathway by acetylsalicylic acid (COX-inhibitor), TxA 2receptor inhibitors, or TxA 2 -synthase inhibitors does not inhibit platelet activation completely. Secreted ADP activates additional Gi-mediated pathways via its P2Y 12 -receptor, leading to inhibition of adenylcyclase with subsequent decrease of the activation blocking messenger cAMP.…”

Section: Procoagulant Activity-model Of Receptor-mediated Thrombin Ge...mentioning

confidence: 99%

Platelets: Physiology and Biochemistry

Jurk,

Kehrel

2023

Semin Thromb Hemost

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This manuscript represents a republication of a manuscript originally published in STH in 2005. This republication is to help celebrate 50 years of publishing for STH. The original abstract follows.Platelets are specialized blood cells that play central roles in physiologic and pathologic processes of hemostasis, inflammation, tumor metastasis, wound healing, and host defense. Activation of platelets is crucial for platelet function that includes a complex interplay of adhesion and signaling molecules. This article gives an overview of the activation processes involved in primary and secondary hemostasis, for example, platelet adhesion, platelet secretion, platelet aggregation, microvesicle formation, and clot retraction/stabilization. In addition, activated platelets are predominantly involved in cross-talk to other blood and vascular cells. Stimulated “sticky” platelets enable recruitment of leukocytes at sites of vascular injury under high shear conditions. Platelet-derived microparticles as well as soluble adhesion molecules, sP-selectin and sCD40L, shed from the surface of activated platelets, are capable of activating, in turn, leukocytes and endothelial cells. This article focuses further on the new view of receptor-mediated thrombin generation of human platelets, necessary for the formation of a stable platelet–fibrin clot during secondary hemostasis. Finally, special emphasis is placed on important stimulatory and inhibitory signaling pathways that modulate platelet function.

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Platelet activation and thrombosis: Studies in a patient with essential thrombocythemia

et al. 1996

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Recent advances permit the detection of activated platelets using specific monoclonal antibodies and flow cytometry. Nevertheless, there are few reports in which activated platelets have been studied over a period of time in patients at risk for thrombosis. Our patient S.D. has essential thrombocythemia and a prothrombotic state manifested in two major thrombotic episodes involving the portal vein and a mesenteric artery. Investigation revealed both spontaneous aggregation and hyperaggregability in response to ADP and the presence of activated platelets in platelet-rich plasma as revealed by flow cytometry. Interestingly, the activated platelets were recognized by an anti-RIBS ("receptor-induced binding site") monoclonal antibody that recognized bound fibrinogen but not by antibodies reactive with antigens whose presence on the platelet surface was secretion dependent. Treatment with aspirin inhibited spontaneous platelet aggregation but had little effect on the activated platelet profile. A change of therapy to ticlopidine suppressed expression of platelet activation markers. Treatment with ticlopidine has continued for 1 year so far without further thrombotic complications.

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Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release

Cited by 114 publications

References 0 publications

Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery

Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery

Platelets: Physiology and Biochemistry

Platelet activation and thrombosis: Studies in a patient with essential thrombocythemia

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