Effect of glycoprotein IIb/IIIa inhibitors on CD62p expression, platelet aggregates, and microparticles in vitro

Matzdorff, Axel; Kühnel, Gitta; Kemkes‐Matthes, B.; Pralle, H.; Voss, Reinhard; Fareed, Jawed

doi:10.1067/mlc.2000.104907

Cited by 29 publications

(18 citation statements)

References 32 publications

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“…This assumption has been supported by studies in animal models [50]. When we used GP IIb/IIIa inhibitors (abciximab, DMP728) to prevent incorporation into aggregates then the number of CD62p-positive platelets increased [51]. The activated platelets did not aggregate but remained in whole blood as singlets.…”

Section: Limitations To the Flow-cytometric Detection Of Platelet Actsupporting

confidence: 51%

Evaluation of Platelet Activation in Coronary Artery Disease – the Role of Flow Cytometry

Matzdorff¹

2000

Transfus Med Hemother

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Within the last decade flow cytometry gave many new insights into the physiology and pathophysiology of platelet activation. This review provides an overview of the different flow-cytometric techniques which have been applied to study platelet activation in patients with coronary artery disease. CD62p is probably the most commonly used platelet activation marker in patients with coronary artery disease. Other antibodies (PAC 1, LIBS1, anti-FGN, etc.) can be utilized to monitor activation of the glycoprotein (GP) IIb/IIIa receptor. The analysis of microparticles, platelet-leukocyte conjugates, and intraplatelet signaling cascades provides additional information on the different steps of platelet activation. However, activation markers do not always adequately reflect the degree of platelet activation. Limitations of flow-cytometric techniques will be discussed. Flow cytometry shows that GP IIb/IIIa activation plays a pivotal role in coronary artery thrombosis which supports the development of GP IIb/IIIa receptor blockers to treat acute coronary syndromes. The GP IIb/IIIa-receptor occupancy assay is one of the first flow-cytometric platelet assays designed to become a part of routine hematology analysis. Flow-cytometric techniques contribute substantially to our understanding of platelet activation during acute coronary syndromes and thus to the development of new drugs and therapeutic approaches.

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Section: Limitations To the Flow-cytometric Detection Of Platelet Actsupporting

confidence: 51%

Evaluation of Platelet Activation in Coronary Artery Disease – the Role of Flow Cytometry

Matzdorff¹

2000

Transfus Med Hemother

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“…Thus, discrepancies occur between exposure of P-selectin on platelets and the numbers of PMPs, which we have found in vitro and others in vivo (6,7,(12)(13)(14). These discrepancies may be attributed, at least in part, to the persistent release of MPs by megakaryocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Because analysis of PMPs does not require fixation and can be applied to stored plasma samples, batchwise analysis of the in vivo platelet activation status is feasible. However, although several studies have confirmed concomitant changes in exposure of platelet Pselectin and circulating numbers of PMPs in vivo (10,11 ), others found discrepancies between both (6,7,(12)(13)(14), which may call into question the relevance of PMP numbers as a marker of platelet activation.…”

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confidence: 99%

P-Selectin- and CD63-Exposing Platelet Microparticles Reflect Platelet Activation in Peripheral Arterial Disease and Myocardial Infarction

et al. 2006

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Background: Platelet-derived microparticles (PMPs) are generally considered a marker of platelet activation in cardiovascular disease. We studied the extent to which PMP subpopulations parallel platelet activation in vitro and in vivo. Methods: Using flow cytometry, we analyzed PMP subpopulations from resting and activated platelets in vitro (n ‫؍‬ 6) as well as from plasma samples of patients with stable angina, peripheral arterial disease, or myocardial infarction [non-ST-elevation (NSTEMI) and ST-elevation (STEMI)] and from older, age-and sexmatched and young healthy individuals [n ‫؍‬ 10 for all groups except NSTEMI (n ‫؍‬ 11)]. Coagulation markers prothrombin fragment F 1 ؉ 2 and thrombin-antithrombin complexes were determined by ELISA. The PMPassociated fraction of soluble (s)P-selectin was estimated by ELISA. Results: In vitro, stimulation of platelets with thrombin receptor-activating peptide (15 mol/L) or the calcium ionophore A23187 (2.5 mol/L) increased fractions of both platelets and PMPs exposing P-selectin or CD63 (P <0.001 for all). Whereas the number of PMPs released by A23187-stimulated platelets increased significantly (P <0.001), the number of PMPs released from thrombin receptor-activating peptide-stimulated platelets remained constant (P >0.05). Ex vivo, numbers of circu-

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“…The analysis of microplatelet fraction after thrombin-induced activation revealed that the lowest statistically significant percentage of CD62P+ and CD63+ platelets occurs in E. granulosus patients. It is likely that microplatelets combine to form larger conglomerates, which are differentiated as platelet aggregates or there may act GP IIb-IIIa inhibitors, produced by the parasite to block microplatelet formation (Matzdorff et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Activation of blood platelets in echinococcosis — CD62P and CD63 expression

et al. 2005

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Effect of glycoprotein IIb/IIIa inhibitors on CD62p expression, platelet aggregates, and microparticles in vitro

Cited by 29 publications

References 32 publications

Evaluation of Platelet Activation in Coronary Artery Disease – the Role of Flow Cytometry

Evaluation of Platelet Activation in Coronary Artery Disease – the Role of Flow Cytometry

P-Selectin- and CD63-Exposing Platelet Microparticles Reflect Platelet Activation in Peripheral Arterial Disease and Myocardial Infarction

Activation of blood platelets in echinococcosis — CD62P and CD63 expression

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