Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin through ERK/p38 MAPKs pathways

Cheng, Gong; Shan, Xuefeng; Wang, Xu-Lang; Wei-wei, Dong; Li, Zhe; Liu, Xinhong; Zhang, Wei; Xing, Kun; Chang, Feng-Jun

doi:10.1111/1755-5922.12273

Cited by 18 publications

(26 citation statements)

References 36 publications

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“…In addition, when MVs and its active substances mediated the activation of the target cell signalling pathway, blocking the transmission of the signalling pathway can alleviate the biological effects caused by MVs. Aspirin partially blocks the inflammatory, oxidative stress, coagulation and adhesion properties of MVs by inhibiting ErK‐NO/O 2 and p38‐NF‐κB‐VCAM‐1 signalling pathways . Losartan, an angiotensin type 1 receptor (AT1 receptor), can inhibit MV‐induced endothelial cell senescence by reducing the expression of mitogen‐activated protein kinase and PI3K .…”

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

confidence: 99%

“…In clinic, some therapeutic drugs, such as aspirin, imipramine, acetylsalicylate and resveratrol, have exhibited obvious effects in reducing the release of MVs in circulation, and their ability to alleviate the progression of diseases to a certain extent. For example, after aspirin treatment, PMVs decreased, and the expression of ERK1/2, p38 MAPKs and JNKs decreased, thereby reducing the damage of MVs to target cells . Aspirin also inhibits the activation of vascular parietal cells by reducing the release of MVs .…”

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

confidence: 99%

“…Aspirin also inhibits the activation of vascular parietal cells by reducing the release of MVs . Resveratrol can reduce the levels of TNF‐α and EMVs in peripheral blood by a cascade of intracellular NF‐κB molecules and has a good effect on vascular endothelial function and systemic inflammation . Acetylsalicylate treatment can reduce the number of circulating endothelial cells and PMVs in patients, and has been widely used in the treatment of cardiovascular diseases .…”

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

confidence: 99%

“…In order to maintain the stability of the internal environment, the MVs to target cells. 68 Aspirin also inhibits the activation of vascular parietal cells by reducing the release of MVs. 77 Resveratrol can reduce the levels of TNF-α and EMVs in peripheral blood by a cascade of intracellular NF-κB molecules and has a good effect on vascular endothelial function and systemic inflammation.…”

Section: Reduce Harmful MV Releasementioning

confidence: 99%

“…77 Resveratrol can reduce the levels of TNF-α and EMVs in peripheral blood by a cascade of intracellular NF-κB molecules and has a good effect on vascular endothelial function and systemic inflammation. 68 Acetylsalicylate treatment can reduce the number of circulating endothelial cells and PMVs in patients, and has been widely used in the treatment of cardiovascular diseases. 78 Studies have shown that the dietary intake of polyunsaturated fatty acids, fruits and vegetables can reduce leucocyte activation, platelet aggregation and MV shedding, thereby reducing the risk of cardiovascular disease and delaying the progression of atherosclerotic thrombosis.…”

Section: Reduce Harmful MV Releasementioning

confidence: 99%

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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%

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

confidence: 99%

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

confidence: 99%

Section: Reduce Harmful MV Releasementioning

confidence: 99%

Section: Reduce Harmful MV Releasementioning

confidence: 99%

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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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Kinetics of Circulating Extracellular Vesicles Over the 24‐Hour Dosing Interval After Low‐Dose Aspirin Administration in Patients at Cardiovascular Risk

Liani

Simeone

Tripaldi

et al. 2023

Clin Pharma and Therapeutics

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Extracellular vesicles (EVs) are small vesicles deriving from all cell types during cell activation, involved in transcellular communication, and regarded as predictors of vascular damage and of cardiovascular events. We tested the hypothesis that, in patients on chronic low-dose aspirin treatment for cardiovascular prevention, aspirin may affect the release of EVs within the 24-hour interval. We enrolled 84 patients, mostly at high or very high cardiovascular risk, on chronic low-dose aspirin treatment. The numbers of circulating EVs (cEVs) and annexinV+ cEVs (total, platelet-derived, endothelial-derived, and leucocyte-derived) were assessed immediately before, and after 10 and 24 hours of a witnessed aspirin administration. Platelet cyclooxygenase 1 (COX-1) recovery was characterized by measuring serum thromboxane B 2 (sTXB 2 ) at the same timepoints. Nine healthy participants were also enrolled. In patients, daily aspirin administration acutely inhibited after 10 hours following aspirin administrations the release of cEVs (total and leukocyte-derived) and annexinV+ cEVs (total, platelet-derived, endothelial-derived, and leukocytederived), with a rapid recovery at 24 hours. The inhibition after 10 hours suggests a COX-1-dependent mechanism. Interestingly, the slope of platelet-derived and of annexinV+ platelet-derived cEVs were both directly related to sTXB 2 slope and COX-1 messenger RNA, raising the hypothesis that vice versa, cEVs may affect the rate of COX-1 recovery and the subsequent duration of aspirin effect. In healthy participants, no circadian difference was observed, except for leukocyte-derived cEVs. Our findings suggest a previously unappreciated effect of aspirin on the kinetics of a subset of cEVs possibly contributing to the cardioprotective effects of this drug.

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Proteomic analysis of extracellular vesicle cargoes mirror the cardioprotective effects of rivaroxaban in patients with venous thromboembolism

Weiss,

Uhrig,

Kelliher

et al. 2024

Proteomics Clinical Apps

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BackgroundVenous thromboembolism (VTE) remains a significant cause of morbidity and mortality worldwide. Rivaroxaban, a direct oral factor Xa inhibitor, mediates anti‐inflammatory and cardiovascular‐protective effects besides its well‐established anticoagulant properties; yet, these remain poorly characterized. Extracellular vesicles (EVs) are considered proinflammatory messengers regulating a myriad of (patho)physiological processes and may be highly relevant to the pathophysiology of VTE. The effects of Rivaroxaban on circulating EVs in VTE patients remain unknown. We have established that differential EV biosignatures are found in patients with non‐valvular atrial fibrillation anticoagulated with Rivaroxaban versus warfarin. Here, we investigated whether differential proteomic profiles of circulating EVs could also be found in patients with VTE.Methods and ResultsWe performed comparative label‐free quantitative proteomic profiling of enriched plasma EVs from VTE patients anticoagulated with either Rivaroxaban or warfarin using a tandem mass spectrometry approach. Of the 182 quantified proteins, six were found to be either exclusive to, or enriched in, Rivaroxaban‐treated patients. Intriguingly, these proteins are involved in negative feedback regulation of inflammatory and coagulation pathways, suggesting that EV proteomic signatures may reflect both Rivaroxaban's anti‐coagulatory and anti‐inflammatory potential.ConclusionsThese differences suggest Rivaroxaban may have pleiotropic effects, supporting the reports of its emerging anti‐inflammatory and cardiovascular‐protective characteristics relative to warfarin.

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Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin through ERK/p38 MAPKs pathways

Abstract: These results indicate that the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs can be partly blocked by aspirin via the ERK-NO/O2- and p38 -NF-κB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.

Cited by 18 publications

References 36 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

Kinetics of Circulating Extracellular Vesicles Over the 24‐Hour Dosing Interval After Low‐Dose Aspirin Administration in Patients at Cardiovascular Risk

Proteomic analysis of extracellular vesicle cargoes mirror the cardioprotective effects of rivaroxaban in patients with venous thromboembolism

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