Microparticles from Patients Undergoing Percutaneous Coronary Intervention Impair Vasodilatation by Uncoupling Endothelial Nitric Oxide Synthase

Yu, Sha; Shan, Xuefeng; Han, Wenqi; Zhang, Qian-Rong; Gao, Jie; Wang, Yi; Sun, Changqing; Zhang, Sui-Long

doi:10.1097/shk.0000000000000823

Cited by 11 publications

(8 citation statements)

References 34 publications

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“…Furthermore, MVs of endothelial origin have shown to decrease nitric oxide (NO) production in vitro ( 22 , 23 ) and under high glucose conditions through changes in oxidative stress ( 24 ) or inducing a temporal cross talk between mitochondria and endoplasmic reticulum ( 25 ). These effects have been obtained in ex vivo studies ( 23 , 26 ) and with patient-derived MVs in pathologies such as myocardial infarction (MI) ( 27 ), end-stage renal failure ( 15 ), metabolic syndrome ( 28 ), valvular heart disease and cardiac injury ( 29 ), and undergoing percutaneous coronary intervention ( 30 ). As a result, vascular tone and endothelial repair capacity are altered.…”

Section: Mv-mediated Regulatory Mechanisms In the Development And Promentioning

confidence: 99%

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Badimon¹,

Suades²,

Arderiu³

et al. 2017

Front. Cardiovasc. Med.

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Atherosclerosis (AT) is a progressive chronic disease involving lipid accumulation, fibrosis, and inflammation in medium and large-sized arteries, and it is the main cause of cardiovascular disease (CVD). AT is caused by dyslipidemia and mediated by both innate and adaptive immune responses. Despite lipid-lowering drugs have shown to decrease the risk of cardiovascular events (CVEs), there is a significant burden of AT-related morbidity and mortality. Identification of subjects at increased risk for CVE as well as discovery of novel therapeutic targets for improved treatment strategies are still unmet clinical needs in CVD. Microvesicles (MVs), small extracellular plasma membrane particles shed by activated and apoptotic cells have been widely linked to the development of CVD. MVs from vascular and resident cells by facilitating exchange of biological information between neighboring cells serve as cellular effectors in the bloodstream and play a key role in all stages of disease progression. This article reviews the current knowledge on the role of MVs in AT and CVD. Attention is focused on novel aspects of MV-mediated regulatory mechanisms from endothelial dysfunction, vascular wall inflammation, oxidative stress, and apoptosis to coagulation and thrombosis in the progression and development of atherothrombosis. MV contribution to vascular remodeling is also discussed, with a particular emphasis on the effect of MVs on the crosstalk between endothelial cells and smooth muscle cells, and their role regulating the active process of AT-driven angiogenesis and neovascularization. This review also highlights the latest findings and main challenges on the potential prognostic, diagnostic, and therapeutic value of cell-derived MVs in CVD. In summary, MVs have emerged as new regulators of biological functions in atherothrombosis and might be instrumental in cardiovascular precision medicine; however, significant efforts are still needed to translate into clinics the latest findings on MV regulation and function.

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Section: Mv-mediated Regulatory Mechanisms In the Development And Promentioning

confidence: 99%

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Badimon¹,

Suades²,

Arderiu³

et al. 2017

Front. Cardiovasc. Med.

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“…For EMPs, Jimenez et al [35] showed that when apoptosis was induced in endothelial cells in-vitro, activation markers on the endothelial cells and cell activation induced CD62E+ EMPs remained stable, while apoptotic markers and the production of apoptotic EMPs increased rapidly. In patients with acute coronary syndrome, three studies have documented a pattern with high concentrations of apoptotic EMPs [35, 55, 56], probably reflecting acute endothelial cell injury due to ischemia, whereas other MP subtypes were not described.…”

Section: Discussionmentioning

confidence: 99%

Changes in microparticle profiles by vitamin D receptor activation in chronic kidney disease – a randomized trial

et al. 2019

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Background Microparticles (MPs) are biomarkers and mediators of disease through their expression of surface receptors, reflecting activation or stress in their parent cells. Endothelial markers, ICAM-1 and VCAM-1, are implicated in atherosclerosis and associated with cardiovascular risk. Chronic kidney disease (CKD) patients have endothelial dysfunction and high levels of endothelial derived MPs. Vitamin D treatment has been reported to ameliorate endothelial function in CKD patients. We aimed to examine cell specific MP profiles and concentrations of MPs expressing the atherosclerotic markers ICAM-1 and VCAM-1 after treatment with paricalcitol in patients with CKD stage 3–4. Methods Sub-study of the previously reported SOLID trial where 36 patients were randomly assigned to placebo, 1 or 2 μg paricalcitol, for 12 weeks. MPs were measured by flow cytometry after labelling with antibodies against endothelial (CD62E), platelet (CD62P, CD41, CD154) leukocyte (CD45) and vascular (CD54, CD106) markers. Results Patients had a mean age of 65 years with a mean eGFR of 40 mL/min/1.73m 2 . Concentrations of ICAM-1 positive MPs were significantly reduced by treatment (repeated measures ANOVA p = 0.04). Repeated measures MANOVA of concentrations of endothelial, platelet and leukocyte MPs showed sustained levels in the 2 μg treatment group ( p = 0.85) but a decline in the 1 μg ( p = 0.04) and placebo groups ( p = 0.005). Conclusions Treatment with paricalcitol reduces concentrations of ICAM-1 positive MPs. This is accompanied by sustained concentrations of all cell specific MPs in the 2 μg group, and decreasing concentrations in the other groups, possibly due to a more healthy and reactive endothelium with paricalcitol treatment.

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“…The level of PMVs was positively associated with the extent of myocardial damage (peak CK-MB: r = 0.408, p = 0.019). Ye et al (2017)…”

Section: Pmvs)mentioning

confidence: 99%

“…For their role in regulating the coagulation cascade and thromboinflammation, identifying circulating PMVs might have a role in stratifying patients at risk of AMI in both primary and secondary prevention setting. High serum levels of circulatory PMVs have been observed in patients with ACS and are also associated with the degree of elevation of cardiac enzymes, inflammatory biomarkers and various markers of myocardial injury(Christersson, Thulin, & Siegbahn, 2017;Cui et al, 2013;Giannopoulos et al, 2014;Hartopo, Puspitawati, Gharini, & Setianto, 2016; Montoro-Garcia et al, 2013;Ye et al, 2017;Table 1)…”

mentioning

confidence: 99%

Update on pathological platelet activation in coronary thrombosis

Elia

Montecucco

Portincasa

et al. 2018

Journal Cellular Physiology

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Although coronary thrombosis (CT) is integral to cardiovascular outcomes, the underlying pathophysiological mechanisms remain unclear. CT may occur in case of atherosclerotic plaque erosion/rupture, or even after stenting implantation. Platelets (PLT) activation is the keystone of atherothrombosis and depends on many dysregulated elements, including endothelial dysfunction, oxidized lipoproteins, and immune response. Besides the classical view of PLT as an effector of hemostatic response, a new repertoire of PLT activities is emerging. PLT lipidome oxidation is a self‐maintaining process which promotes PLT reactivity, coagulation cascade, and inflammatory cell activation. PLT‐innate immune cell interaction is also sustained by neutrophil extracellular traps and NLRP3 inflammasome pathways. Other noteworthy emerging mechanisms are implicated in the crosstalk between PLT and surrounding cells. Especially, microvesicles (MVs) released from PLT may extend their signaling network far beyond the classical cell−cell interactions. Moreover, the recognition of noncoding RNA in PLT MVs introduce another layer of complexity in terms of intercellular signaling by a direct regulation of messenger RNA profile and gene expression in the recipient cells. The aim of this narrative review is to update the recent advance in CT and intracoronary stent thrombosis, including causal factors and potential translation of experimental evidence into the clinical setting.

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Microparticles from Patients Undergoing Percutaneous Coronary Intervention Impair Vasodilatation by Uncoupling Endothelial Nitric Oxide Synthase

Abstract: PCI further enhances the vascular injury effect of MPs. Circulating MPs may be a potential therapeutic target for patients undergoing PCI.

Cited by 11 publications

References 34 publications

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Changes in microparticle profiles by vitamin D receptor activation in chronic kidney disease – a randomized trial

Update on pathological platelet activation in coronary thrombosis

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