Dynamic microvesicle release and clearance within the cardiovascular system: triggers and mechanisms

Ayers, Lisa; Nieuwland, Rienk; Kohler, Malcolm; Kraenkel, Nicolle; Ferry, Berne; Leeson, Paul

doi:10.1042/cs20140623

Cited by 58 publications

(59 citation statements)

References 145 publications

(179 reference statements)

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“…In order to maintain the stability of the internal environment, the body can remove these MVs to a certain extent, thereby reducing the adverse effects of MVs on cells and organs. Microvesicles from different cell sources in circulation can bind to cells that mediate its clearance and remove through the liver, spleen and lungs . The clearance of MVs is associated with its surfactants and receptors expressed on the cell surface.…”

Section: Effective Ways Of Blocking Cell Damage Mediated By Mvs and Imentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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Cell‐derived microvesicles are membrane vesicles produced by the outward budding of the plasma membrane and released by almost all types of cells. These have been considered as another mechanism of intercellular communication, because they carry active molecules, such as proteins, lipids and nucleic acids. Furthermore, these are present in circulating fluids, such as blood and urine, and are closely correlated to the progression of pathophysiological conditions in many diseases. Recent studies have revealed that microvesicles have a dual effect of damage and protection of receptor cells. However, the nature of the active molecules involved in this effect remains unclear. The present study mainly emphasized the mechanism of microvesicles and the active molecules mediating the different biological effects of receptor cells by affecting autophagy, apoptosis and inflammation pathways. The effective ways of blocking microvesicles and its active molecules in mediating cell damage when microvesicles exert harmful effects were also discussed.

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Section: Effective Ways Of Blocking Cell Damage Mediated By Mvs and Imentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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“…Clearance occurs predominantly by phagocytosis, endocytosis, micropinocytosis and membrane fusion (Ayers et al 2015). Clearance occurs predominantly by phagocytosis, endocytosis, micropinocytosis and membrane fusion (Ayers et al 2015).…”

Section: Baselinementioning

confidence: 99%

Passive heat stress reduces circulating endothelial and platelet microparticles

Bain

Ainslie

Bammert

et al. 2017

Experimental Physiology

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What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial- and platelet-derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial- and platelet-derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non-pathological hyperthermia. Interest in circulating endothelial- and platelet-derived microparticles (EMPs and PMPs, respectively) has increased because of their potential pathogenic role in vascular disease and as biomarkers for vascular health. Hyperthermia is commonly associated with a pro-inflammatory stress but might also provide vascular protection when the temperature elevation is non-pathological. Circulating microparticles might contribute to the cellular adjustments and resultant vascular impacts of hyperthermia. Here, we determined whether circulating concentrations of arterial EMPs and PMPs are altered by passive heat stress (+2°C oesophageal temperature). Ten healthy young men (age 23 ± 3 years) completed the study. Hyperthermia was achieved by circulating ∼49°C water through a water-perfused suit that covered the entire body except the hands, feet and head. Arterial (radial) blood samples were obtained immediately before heating (normothermia) and in hyperthermia. The mean ± SD oesophageal temperature in normothermia was 37.2 ± 0.1°C and in hyperthermia 39.1 ± 0.1°C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by ∼30% (mean ± SD; from 61 ± 8 to 43 ± 7 microparticles μl ; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl ; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl ). These beneficial reductions in circulating EMPs and PMPs in response to a 2°C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.

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“…Recently, aphaeresis-derived pMVs were shown to circulate for more than 5 h (Rank et al, 2010), increasing the discrepancy in pMV turnover, which may rely on distinct fate signals due to secretion process (Dasgupta et al, 2009; Abdel-Monem et al, 2010). Indeed, levels of pMVs might reflect the balance between dynamic mechanisms for release and clearance (Ayers et al, 2015). …”

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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Dynamic microvesicle release and clearance within the cardiovascular system: triggers and mechanisms

Cited by 58 publications

References 145 publications

The role of microvesicles and its active molecules in regulating cellular biology

The role of microvesicles and its active molecules in regulating cellular biology

Passive heat stress reduces circulating endothelial and platelet microparticles

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

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