P-Selectin expression, platelet aggregates, and platelet-derived microparticle formation are increased in peripheral arterial disease

Zeiger, F; Stephan, Susanne; Hoheisel, G; Pfeiffer, Doris; Ruehlmann, C; Koksch, Mario

doi:10.1097/00001721-200012000-00005

Cited by 91 publications

(67 citation statements)

References 24 publications

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“…Platelet microparticles (PMP) are small vesicles that are released from activated platelets. They are encountered in a variety of clinical settings, including arterial thrombosis and peripheral vascular disease [3], hypertension, diabetes, stroke [4][5][6], and ather osclerosis [7]. PMP enhance thrombus formation [8,9] and contribute to platelet activation [10].…”

Section: Introductionmentioning

confidence: 99%

Expression of complement components and inhibitors on platelet microparticles

2008

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Platelet microparticles (PMP) are released from activated platelets and play an important role in hemostasis, thrombosis and inflammation. Since platelets were recently found to demonstrate an intrinsic capacity for activating both classical and alternative pathways of the complement system, the present study extended these observations to PMP. PMP were generated by treating platelets with 10 µM A23187 (37°C, 5 min). PMP were identified by flow cytometry, based on size, Annexin V binding, and expression of P-selectin and GPIIb (CD41). PMP expressed gC1qR/p33, a multifunctional cellular protein that was recently described to activate the classical complement cascade. PMP also expressed the classical pathway and contact system regulator, CI inhibitor (C1-INH), as well as CD55 and CD59. Despite C1-INH expression, PMP supported classical pathway C4 activation in the presence of purified C1 and C4. Moreover, statistically significant deposition of C3b and C5b-9 was detected on PMP exposed to plasma, concurrently with expression of CD55 and CD59. These data provide the first evidence for the ability of PMP to support in situ complement activation. Complement activation contributes to a variety of vascular and inflammatory disease states including atherosclerosis and ischemia/reperfusion injury.

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Section: Introductionmentioning

confidence: 99%

Expression of complement components and inhibitors on platelet microparticles

2008

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“…[8][9][10] Elevated numbers of circulating microparticles have been found in patients with a great variety of diseases with vascular involvement and hypercoagulability. [11][12][13][14][15] To the best of our knowledge, there are no reported studies that evaluated circulating microparticles in impotent diabetic men. Therefore, the aims of this study were (a) to evaluate circulating endothelial (EMP) and platelet microparticles (PMP) in diabetic men with ED, (b) to address the relation between circulating microparticles and the severity of ED and (c) to assess the relation between circulating microparticles and endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Endothelial microparticles correlate with erectile dysfunction in diabetic men

et al. 2006

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Cell-derived microparticles are supposed to be involved in endothelial dysfunction and atherogenesis. This study aimed to evaluate circulating microparticles in diabetic subjects with erectile dysfunction (ED) and their relation with endothelial dysfunction. Thirty diabetic men with ED and 20 age-matched control subjects without ED were assessed for circulating microparticles and endothelial dysfunction. Flow cytometry was used to assess microparticles by quantification of circulating endothelial (EMP, CD31 þ /CD42b À ) and platelet (PMP, CD31 þ /CD42b þ ) microparticles in peripheral blood. Endothelium-dependent flow-mediated dilation (FMD) was evaluated in the right brachial artery after reactive hyperemia. Compared with non-diabetic subjects, diabetic men presented significantly higher numbers of EMP (P ¼ 0.001), and reduced FMD (P ¼ 0.01), with a significant inverse correlation between the number of circulating EMP and the International Index of Erectile Function (IIEF) score (r ¼ À0.457, P ¼ 0.01). Multivariate analysis correcting for age, anthropometric indices, glucose and lipid parameters, FMD and PMP identified EMP as the only independent predictor for IIEF score (P ¼ 0.03). EMP are elevated in impotent diabetic subjects and independently involved in the pathogenesis of ED.

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“…Therefore, the numbers of circulating PMPs reflect the platelet activation status in vivo, for example, in patients with peripheral arterial disease (5 ), unstable angina (6 ), myocardial infarction (MI) (7 ), cerebrovascular accident (8,9 ), and diabetes (9 ). 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.…”

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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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P-Selectin expression, platelet aggregates, and platelet-derived microparticle formation are increased in peripheral arterial disease

Cited by 91 publications

References 24 publications

Expression of complement components and inhibitors on platelet microparticles

Expression of complement components and inhibitors on platelet microparticles

Endothelial microparticles correlate with erectile dysfunction in diabetic men

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

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