Platelet glycoprotein IIb/IIIa blockade with tirofiban: effect on aggregation caused by P256, an antibody to human IIb/IIIa receptors

Fisher, Ian; Robinson, Paul; Ritter, James M.

doi:10.1046/j.1365-2125.1999.00990.x

Cited by 5 publications

(3 citation statements)

References 8 publications

(7 reference statements)

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“…These data suggest that platelets under activated condition regulate immune response of monocytes rather than platelets under steady-state condition. Tirofiban is a GP IIb/IIIa-specific antagonist and is capable of blocking GP IIb/IIIa-mediated platelet activation and aggregation ( Fisher et al., 1999 ; Tummala and Rai, 2021 ). Our data showed that tirofiban inhibited platelet aggregation and removed the elevated phagocytosis effect and expression of inflammatory cytokine in PRP-treated THP-1 cells.…”

Section: Discussionmentioning

confidence: 99%

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

Zheng

Duan

Tang

et al. 2021

Front. Cell. Infect. Microbiol.

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Candida albicans is the most common fungal pathogen in humans, causing invasive disease and even potentially life-threatening systemic infections when tissue homeostasis is disrupted. Previous studies have identified an essential role of platelets in infection and immunity, especially when they are activated. However, it is still unclear whether platelets can be activated by C. albicans, and even less is known about the role of platelets in C. albicans infection. Herein, we showed that C. albicans induced platelet activation in vitro. C. albicans elevated the levels of AKT Ser473 phosphorylation, and inhibition of the PI3K-AKT signaling pathway reversed C. albicans-induced platelet activation. Surprisingly, C. albicans-induced platelet activation occurred in an integrin glycoprotein (GP) IIb/IIIa-dependent manner but was independent of the pattern recognition receptors toll-like receptor (TLR) 2 and TLR4. Interestingly, platelets enhanced the phagocytosis of human monocytes challenged with C. albicans and upregulated the expression of inflammatory cytokines, which were dependent on platelet activation mediated by GP IIb/IIIa. The present work provides new insights into the role of activated platelets in the defense against C. albicans, highlighting the importance of GP IIb/IIIa in the recognition of C. albicans.

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Section: Discussionmentioning

confidence: 99%

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

Zheng

Duan

Tang

et al. 2021

Front. Cell. Infect. Microbiol.

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“…e . fibrinogen binding) [ 41 ] did not prevent the stimulation of OxPhos induced by thrombin, indicating that platelet aggregation through fibrinogen bridges is not a prerequisite for the stimulation of OxPhos induced by thrombin. Similarly, it became clear that thrombin-mediated thromboxane formation through cyclooxygenase activity was not involved in the energetic stimulation by thrombin, as aspirin did not perturb the thrombin-mediated stimulation of OxPhos.…”

Section: Discussionmentioning

confidence: 99%

Glycoprotein Ib activation by thrombin stimulates the energy metabolism in human platelets

Peña¹,

Gutiérrez‐Aguilar

Hernández‐Reséndiz

et al. 2017

PLoS ONE

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Thrombin-induced platelet activation requires substantial amounts of ATP. However, the specific contribution of each ATP-generating pathway i.e., oxidative phosphorylation (OxPhos) versus glycolysis and the biochemical mechanisms involved in the thrombin-induced activation of energy metabolism remain unclear. Here we report an integral analysis on the role of both energy pathways in human platelets activated by several agonists, and the signal transducing mechanisms associated with such activation. We found that thrombin, Trap-6, arachidonic acid, collagen, A23187, epinephrine and ADP significantly increased glycolytic flux (3–38 times vs. non-activated platelets) whereas ristocetin was ineffective. OxPhos (33 times) and mitochondrial transmembrane potential (88%) were increased only by thrombin. OxPhos was the main source of ATP in thrombin-activated platelets, whereas in platelets activated by any of the other agonists, glycolysis was the principal ATP supplier. In order to establish the biochemical mechanisms involved in the thrombin-induced OxPhos activation in platelets, several signaling pathways associated with mitochondrial activation were analyzed. Wortmannin and LY294002 (PI3K/Akt pathway inhibitors), ristocetin and heparin (GPIb inhibitors) as well as resveratrol, ATP (calcium-release inhibitors) and PP1 (Tyr-phosphorylation inhibitor) prevented the thrombin-induced platelet activation. These results suggest that thrombin activates OxPhos and glycolysis through GPIb-dependent signaling involving PI3K and Akt activation, calcium mobilization and protein phosphorylation.

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“…Tirofiban (Aggrastat) is a tyrosine derivative that inhibits fibrinogen binding to GP IIa/IIIb. This particular drug is an Arg-Gly-Asp (RGD)-based peptidomimetic that effectively blocks the surface glycoprotein GPIIb/IIIa receptor reducing thrombin generation and subsequently platelet aggregation and secretion. , The drug is used intravenously together with heparin for coronary applications (unstable angina, non-Q-wave MI, and angioplasty) but not in patients who have hypertension or have had hemorrhagic stroke or suffered trauma. The use of tirofiban with heparin resulted in a significant decrease in the composite endpoints of death, MI, and refractory ischemia. − However, the benefit was short term for patients with acute coronary syndromes.…”

Section: Antiplatelet and Anticoagulant Agents In Cardiovascular Medi...mentioning

confidence: 99%

Anticoagulant and Antiplatelet Agents: Their Clinical and Device Application(s) Together with Usages to Engineer Surfaces

et al. 2004

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An essential aspect of the treatment of patients with cardiovascular disease is the use of anticoagulant and antiplatelet agents for the prevention of further ischaemic events and vascular death resulting from thrombosis. Aspirin and heparin have been the standard therapy for the management of such conditions to date. Recently, numerous more potent platelet inhibitors together with anticoagulant agents have been developed and tested in randomized clinical trials. This article reviews the current state of the art of antiplatelet and anticoagulant therapy in light of its potential clinical efficacy. It then focuses on the usages of these agents in order to improve the performance of clinical devices such as balloon catheters, coronary stents, and femoropopliteal bypass grafting and extra corporeal circuits for cardiopulmonary bypass. The article then goes on to look at the usage of these agents more specifically heparin, heparan, hirudin, and coumarin in the development of more biocompatible scaffolds for tissue engineering.

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Platelet glycoprotein IIb/IIIa blockade with tirofiban: effect on aggregation caused by P256, an antibody to human IIb/IIIa receptors

Cited by 5 publications

References 8 publications

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

Glycoprotein Ib activation by thrombin stimulates the energy metabolism in human platelets

Anticoagulant and Antiplatelet Agents: Their Clinical and Device Application(s) Together with Usages to Engineer Surfaces

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