PROTEOMIC ASSESSMENT OF CIRCULATING MICROPARTICLES IN HYPERTENSION AND DIABETES

SummaryCirculating blood microparticles are likely to play a significant role as messengers of biological information. Their accurate quantification and characterisation is challenging and needs to be carefully designed with preferable usage of fresh minimally-processed blood samples. Utilisation of flow cytometers specifically designed for analysis of small-size particles is likely to provide considerable methodological advantages and should be the preferable option. This viewpoint manuscript provides a critical summary of the key methodological aspects of microparticle analysis.Note: The review process for this viewpoint article was fully handled by Christian Weber, Editor in Chief.

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Circulating Endothelial Microparticles: A Key Hallmark of Atherosclerosis Progression

Scientifica ◽

10.1155/2016/8514056 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 19

Author(s):

Keshav Raj Paudel ◽

Nisha Panth ◽

Dong-Wook Kim

Keyword(s):

Vascular Function ◽

Cell Activation ◽

Vascular Inflammation ◽

Rho Kinase ◽

Disease Status ◽

Endothelial Microparticles ◽

Atherosclerosis Progression ◽

Mitogen Activated Protein ◽

Circulating Microparticles ◽

Ros Formation

The levels of circulating microparticles (MPs) are raised in various cardiovascular diseases. Their increased level in plasma is regarded as a biomarker of alteration in vascular function. The prominent MPs present in blood are endothelial microparticles (EMPs) described as complex submicron (0.1 to 1.0 μm) vesicles like structure, released in response to endothelium cell activation or apoptosis. EMPs possess both physiological and pathological effects and may promote oxidative stress and vascular inflammation. EMPs release is triggered by inducer like angiotensin II, lipopolysaccharide, and hydrogen peroxide leading to the progression of atherosclerosis. However, there are multiple physiological pathways for EMPs generation like NADPH oxidase derived endothelial ROS formation, Rho kinase pathway, and mitogen-activated protein kinases. Endothelial dysfunction is a key initiating event in atherosclerotic plaque formation. Atheroemboli, resulting from ruptured carotid plaques, is a major cause of stroke. Increasing evidence suggests that EMPs play an important role in the pathogenesis of cardiovascular disease, acting as a marker of damage, either exacerbating disease progression or triggering a repair response. In this regard, it has been suggested that EMPs have the potential to act as biomarkers of disease status. This review aims to provide updated information of EMPs in relation to atherosclerosis pathogenesis.

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Increased circulating microparticles in streptozotocin‐induced diabetes propagate inflammation contributing to microvascular dysfunction

The Journal of Physiology ◽

10.1113/jp277312 ◽

2019 ◽

Vol 597 (3) ◽

pp. 781-798 ◽

Cited By ~ 3

Author(s):

Qilong Feng ◽

Christian J. Stork ◽

Sulei Xu ◽

Dong Yuan ◽

Xinghai Xia ◽

...

Keyword(s):

Microvascular Dysfunction ◽

Circulating Microparticles ◽

Streptozotocin Induced Diabetes

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Circulating microparticles in carriers of factor V Leiden with and without a history of venous thrombosis

Thrombosis and Haemostasis ◽

10.1160/th12-05-0280 ◽

2012 ◽

Vol 108 (10) ◽

pp. 633-639 ◽

Cited By ~ 16

Author(s):

Elena Campello ◽

Luca Spiezia ◽

Claudia M. Radu ◽

Maria Bon ◽

Sabrina Gavasso ◽

...

Keyword(s):

Factor V Leiden ◽

Annexin V ◽

Factor V ◽

Thrombotic Risk ◽

Study Results ◽

Significant Difference ◽

Circulating Microparticles ◽

Venous Thromboembolic ◽

The Mean ◽

And Gender

SummaryAlthough factor V Leiden (FVL) is a major determinant of thrombotic risk, the reason why less than 10% of carriers eventually develop venous thromboembolic (VTE) events is unknown. Recent observations suggest that circulating levels of microparticles (MP) may contribute to the thrombogenic profile of FVL carriers. We measured the plasma level of annexin V-MP (AMP) platelet-MP (PMP), endothelial-MP (EMP), leukocyte-MP (LMP) and tissue factor-bearing MP (TF+MP), and the MP procoagulant activity (PPL) in 142 carriers of FVL (of these 30 homozygous and 49 with prior VTE), and in 142 age and gender-matched healthy individuals. The mean (± SD) level of AMP was 2,802 ± 853 MP/ μl in carriers and 1,682 ± 897 in controls (p<0.0001). A statistically significant difference between homozygous and heterozygous carriers of FVL was seen in the level of PMP, EMP and LMP, but not in that of the remaining parameters. When the analysis was confined to carriers with and without a VTE history, the mean level of AMP was 3,110 ± 791 MP/ μl in the former, and 2,615 ± 839 MP/μl in the latter (p<0.005). The mean level of all subtypes of circulating MP showed a similar pattern. The PPL clotting time was 39 ± 9 seconds (sec) in carriers, and 52 ± 15 sec in controls (p=0.003); and was 35 ± 8 sec in carriers with prior thrombosis, and 41 ± 10 sec in thrombosis-free carriers (p<0.005). Our study results suggest that circulating MP may contribute to the development of thrombosis in carriers of FVL mutation.

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