The Role of Platelet Microparticles in Hemostasis

Owens, Michael R.

doi:10.1016/s0887-7963(94)70096-1

Cited by 44 publications

(20 citation statements)

References 35 publications

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“…According to the previous studies, FVa that expressed on activated Plts could be protected from inactivation by APC. Further experiments also demonstrated that the platelet-derived MPs resulted in increased levels/rates of the cofactor inactivation suppressing the apparent protection developed by intact Plts [41]. This is an important point to take into consideration since elevated levels of circulating MPs have been reported in patients diagnosed with FVL [19].…”

Section: Pathophysiology Of Factor V: Factor V Leiden Mutationmentioning

confidence: 99%

“…Microparticles are small portions of membrane shed from activated cells such as endothelial, monocytes, and/or platelets which support procoagulant activity and contribute to the formation of the hemostatic plug [41, 56–58]. In 2004, Lopez et al [45, 59] proposed a model based on monocytes/macrophages derived microvesicles (MVs) bearing TF with the ability to fuse with activated endothelial cells due to inflammation and promote the initiation of blood coagulation.…”

Section: Pathophysiology Of Inflammation: Role Of Endothelial Dysfmentioning

confidence: 99%

“…The higher number of MPs loaded with proinflammatory components (FV and TF) leads to a procoagulant state which may be more intense in patients with FVL developing the inflammatory episodes described in this paper [41]. Taking into consideration all the findings reviewed above, it seems reasonable to consider that patients diagnosed with FVL will be exposed to enhanced inflammatory responses in sepsis, infection, or IBD not only due to the FVL itself but also for the high presence of MPs with procoagulant properties.…”

Section: Final Considerationsmentioning

confidence: 99%

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Factor V Leiden and Inflammation

2012

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Factor V Leiden, is a variant of human factor V (FV), also known as proaccelerin, which leads to a hypercoagulable state. Along these years, factor V Leiden (FVL) has been studied from the pathophysiologic point of view, and research has been focused on finding clinical approaches for the management of the FVL associated to a trombophilic state. Less attention has been paid about the possible role of FVL in inflammatory conditions known to be present in different disorders such as uremia, cirrhosis, liver transplantation, depression as well as sepsis, infection or, inflammatory bowel disease (IBD). Whether platelet FVL will increase the activation of coagulation and/or in which proportion is able to determine the final outcome in the previously mentioned inflammatory conditions is a subject that remains uncertain. This paper will review the association of FVL with inflammation. Specifically, it will analyze the important role of the endothelium and the contribution of other inflammatory components involved at both the immune and vascular levels. This paper will also try to emphasize the importance of being a FVL carrier in associations to diseases where a chronic inflammation occurs, and how this condition may be determinant in the progression and outcome of a specific clinic situation.

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Section: Pathophysiology Of Factor V: Factor V Leiden Mutationmentioning

confidence: 99%

Section: Pathophysiology Of Inflammation: Role Of Endothelial Dysfmentioning

confidence: 99%

Section: Final Considerationsmentioning

confidence: 99%

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Factor V Leiden and Inflammation

2012

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“…Indeed, previous studies with patients with genetic defects have shown that impaired platelet PCA is translated into reduced vesicle formation (Sims et al, 1989; Gemmell et al, 1993). Despite the mechanisms by which MVs are formed are not well-known yet, pMVs are specifically shed from the platelet plasma membrane by an exocytic budding process (Holme et al, 1993), which involves increases in intracellular calcium, cytoskeleton reorganization (Yano et al, 1994; Pasquet et al, 1996) and changes in membrane lipid asymmetry, and is triggered by physical stimuli (shear stress, hypoxia) (Gemmell et al, 1993; Takano et al, 2004), by a variety of specific agonists (in an additive or even synergistic way; Xiao et al, 2002) or by platelet prolonged storage without agonist/stimuli requirement (Owens, 1994). While most non-physiologic agonists like calcium ionophore are the most potent inducers of MVs, the order of potency of physiologic agonists is C5b-9 membrane attack complex >thrombin plus collagen >thrombin >collagen >adenosine diphosphate >epinephrine (Connor et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Role of Platelet-Derived Microvesicles As Crosstalk Mediators in Atherothrombosis and Future Pharmacology Targets: A Link between Inflammation, Atherosclerosis, and Thrombosis

Suades²,

et al. 2016

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Reports in the last decade have suggested that the role of platelets in atherosclerosis and its thrombotic complications may be mediated, in part, by local secretion of platelet-derived microvesicles (pMVs), small cell blebs released during the platelet activation process. MVs are the most abundant cell-derived microvesicle subtype in the circulation. High concentrations of circulating MVs have been reported in patients with atherosclerosis, acute vascular syndromes, and/or diabetes mellitus, suggesting a potential correlation between the quantity of microvesicles and the clinical severity of the atherosclerotic disease. pMVs are considered to be biomarkers of disease but new information indicates that pMVs are also involved in signaling functions. pMVs evoke or promote haemostatic and inflammatory responses, neovascularization, cell survival, and apoptosis, processes involved in the pathophysiology of cardiovascular disease. This review is focused on the complex cross-talk between platelet-derived microvesicles, inflammatory cells and vascular elements and their relevance in the development of the atherosclerotic disease and its clinical outcomes, providing an updated state-of-the art of pMV involvement in atherothrombosis and pMV potential use as therapeutic agent influencing cardiovascular biomedicine in the future.

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“…The clinical significance of procoagulant activity presented by MV has been the main focus of interest for many studies and has been recently reviewed (68). The relationship between the variable levels of circulating MV and the hemostatic status of the patient has been reported in several hematologic disorders, e.g., immune thrombocytopenic purpura (ITP), heparin-induced thrombocytopenia (HIT), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and disseminated intravascular coagulation (DIC) (43,44,52,69).…”

Section: Hemostatic and Thrombotic-effectsmentioning

confidence: 99%

State-of-the-Art-Review: Microvesicles in Blood Components: Laboratory and Clinical Aspects

Krailadsiri¹,

Seghatchian²,

Bode

1997

Clin Appl Thromb Hemost

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There is ample evidence for the presence of microvesicles (MV) of different sizes and functions in various blood components. A variety of mechanisms have been proposed for the formation of MV. These include mechanical injury, shear stress, cell activation, activation of complements, hypoxia, and the cell aging process. While MV share many biological properties and surface receptors of their parental cells, they demonstrate significant differences in membrane asymmetry of the inner membrane phospholipid, in particular phosphatidylserine (PS). This provides high-affinity binding sites for the components of the prothrombinase complex. To what extent these MV contribute to hemostatic effectiveness, immudomodulation, and some untoward effects of the transfused blood components remains to be fully elucidated. Several methods for qualitative and semiquantitative characterization of MV are now available. Although in most cases it is necessary to separate MV from the intact cells for improved characterization, recent advances in flow cytometry make it possible to accurately differentiate MV in the presence of their parental cells on the basis of light scattering and fluorescent intensity. This review focuses on four main areas of MV in blood components: (1) the proposed mechanisms of platelet vesiculation, (2) factors influencing the formation of MV, (3) laboratory analysis of MV, and (4) the clinical impact of the presence of MV in blood components.

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The Role of Platelet Microparticles in Hemostasis

Cited by 44 publications

References 35 publications

Factor V Leiden and Inflammation

Factor V Leiden and Inflammation

Role of Platelet-Derived Microvesicles As Crosstalk Mediators in Atherothrombosis and Future Pharmacology Targets: A Link between Inflammation, Atherosclerosis, and Thrombosis

State-of-the-Art-Review: Microvesicles in Blood Components: Laboratory and Clinical Aspects

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