Article

The involvement of circulating microparticles in inflammation, coagulation and cardiovascular diseases

Department of Internal Medicine, University of Bologna and S Orsola-Malpighi Hospital, Italy.
The Canadian journal of cardiology (Impact Factor: 3.94). 04/2010; 26(4):140-5. DOI: 10.1016/S0828-282X(10)70371-8
Source: PubMed

ABSTRACT Microparticles (MPs) are small vesicles, ranging in size from 0.1 microm to 2 microm, originating from plasma membranes of endothelial cells, platelets, leukocytes and erythrocytes. MPs can transfer antigens and receptors to cell types that are different from their cell of origin. Circulating MPs provide a procoagulant aminophospholipid surface for the assembly of the specific enzymes of coagulation. Both tissue factor and phosphatidylserine are exposed on MP outer membranes. In addition, MPs can play a significant role in vascular function and inflammation by modulating nitric oxide and prostacyclin production in endothelial cells, and stimulating cytokine release and tissue factor induction in endothelial cells, as well as monocyte chemotaxis and adherence to the endothelium. Finally, increased levels of MPs have been found in the presence of acute coronary syndromes, ischemic stroke, diabetes, systemic and pulmonary hypertension, and hypertriglyceridemia. From a practical point of view, MPs could be considered to be important markers of cardiovascular risk, as well as surrogate end points for assessing the efficacy of new drugs and therapies.

1 Follower
 · 
155 Views
 · 
0 Downloads
  • Source
    • "Other in vitro and in vivo studies have also shown effects on the expression of intracellular miRNAs from PM (Bleck et al., 2013; Fossati et al., 2014) or other exposures that include PM, such as diesel exhaust (Yamamoto et al., 2013) or tobacco smoking (De Flora et al., 2012; Maccani et al., 2010). Although the mechanisms linking air pollution and pulmonary inflammatory responses to vascular diseases are currently unknown, MVs are a plausible link because they can be produced by the respiratory system (Kesimer et al., 2009), can be disseminated through the circulatory system (Orozco and Lewis, 2010) and can lead to cardiovascular dysfunction (Puddu et al., 2010). We investigated the hypothesis that PM and PMassociated metals could modify specific MV-associated miRNAs from plasma. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cardiovascular disease risk has been consistently linked with particulate matter (PM) exposure. Cell-derived microvesicles (MVs) are released into plasma and transfer microRNAs (miRNAs) between tissues. MVs can be produced by the respiratory system in response to proinflammatory triggers, enter the circulatory system and remotely modify gene expression in cardiovascular tissues. However, whether PM affects MV signaling has never been investigated. In this study, we evaluated expression of microRNAs contained within plasma MVs upon PM exposure both in vivo and in vitro. In the in vivo study, we isolated plasma MVs from healthy steel plant workers before and after workplace PM exposure. We measured the expression of 88 MV-associated miRNAs by real-time polymerase chain reaction. To assess a possible source of the MV miRNAs identified in vivo, we measured their miRNA expression in PM-treated A549 pulmonary cell lines in vitro. MiRNA profiling of plasma MVs showed 5.62- and 13.95-fold increased expression of miR-128 and miR-302c, respectively, after 3 days of workplace PM exposure (P < 0.001). According to Ingenuity Pathway Analysis, miR-128 is part of coronary artery disease pathways, and miR-302c is part of coronary artery disease, cardiac hypertrophy and heart failure pathways. In vitro experiments confirmed a dose-dependent expression of miR-128 in MVs released from A549 cells after 6 h of PM treatment (P = 0.030). MiR-302c was expressed neither from A549 cells nor in reference lung RNA. These results suggest novel PM-activated molecular mechanisms that may mediate the effects of air pollution and could lead to the identification of new diagnostic and therapeutic interventions. Copyright © 2014 The Authors. Journal of Applied Toxicology Published by John Wiley & Sons Ltd.
    Journal of Applied Toxicology 01/2015; 35(1). DOI:10.1002/jat.2987 · 3.17 Impact Factor
  • Source
    • "As demonstrated previously, monocytes and macrophages are primary sources of circulating TF via the shedding of TF-bearing MPs41. These MPs, which have PSGP-1 on their surface, participate in platelet thrombus formation not merely by binding to P-selectin on activated platelets67 but by fusing with these platelets via PSGL-1, transferring lipids and proteins, including TF, into their plasma membranes71. "
    [Show abstract] [Hide abstract]
    ABSTRACT: M Microparticles are small membrane fragments shed primarily from blood and endothelial cells during either activation or apoptosis. There is mounting evidence suggesting that microparticles perform a large array of biological functions and contribute to various diseases. Of these disease processes, a significant link has been established between microparticles and venous thromboembolism. Advances in research on the role of microparticles in thrombosis have yielded crucial insights into possible mechanisms, diagnoses and therapeutic targets of venous thromboembolism. In this review, we discuss the definition and properties of microparticles and venous thromboembolism, provide a synopsis of the evidence detailing the contributions of microparticles to venous thromboembolism, and propose potential mechanisms, by which venous thromboembolism occurs. Moreover, we illustrate a possible role of microparticles in cancer-related venous thromboembolism.
    Acta Pharmacologica Sinica 08/2014; 35(9). DOI:10.1038/aps.2014.73 · 2.50 Impact Factor
  • Source
    • "Microparticles (MPs) shed from activated or apoptotic cells contain complex procoagulant and proinflammatory properties.1)2) MPs released from various vascular or peripheral blood cells circulate in the blood and can be sequestered in complicated atherosclerotic plaques. "
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the effect of the additional use of abciximab during percutaneous coronary intervention (PCI) on the level of procoagulant microparticles (MPs) in patients with ST-segment elevation myocardial infarction (STEMI) who had undergone primary PCI. In this study, we studied 86 patients with STEMI (72 men, age 58±13) who had undergone primary PCI. The decision to administer abciximab immediately prior to PCI was left to the discretion of the operator. Blood samples for analysis of MPs were obtained from the femoral artery before and after PCI. MPs with procoagulant potential were measured using a commercial kit. The cellular origins of MPs were determined by antigenic capture with specific antibodies. Procoagulant MPs captured onto annexin V were not changed significantly after PCI {13.4±13.2 nM vs. 13.2±16.1 nM phosphatidylserine equivalent (PS eq), p=0.479}. Abciximab was used in 30 of 86 patients (35%) immediately prior to PCI. In patients who had undergone PCI without abciximab, no significant change in the level of MPs was observed after PCI. However, in the abciximab group, the level of circulating MPs was significantly decreased after PCI (12.0±10.7 nM vs. 7.8±11.7 nM PS eq, p=0.018). Levels of endothelial- and platelet-derived MPs also showed a significant reduction after PCI in the abciximab group. Primary PCI with additional abciximab significantly reduced the level of procoagulant MPs regardless of their cellular origins in patients with STEMI.
    Korean Circulation Journal 09/2013; 43(9):600-6. DOI:10.4070/kcj.2013.43.9.600
Show more

Preview

Download
0 Downloads
Available from