Microparticles: A Novel Player in Cardiovascular Diseases

Durante, Alessandro; Zalewski, J

doi:10.1159/000437045

Cited by 3 publications

(3 citation statements)

References 19 publications

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“…Finally of particular note is the female-specific demethylation of the well known anti-apoptotic gene BCL2L1 (BCL2-like 1), which plays a key role in the regulation of platelet activation and apoptosis 33 . Among the consequences of platelet apoptosis is the production of microparticles, which are recognised to play an important role in inflammation, CVD, coagulation and angiogenesis 34 .…”

Section: Discussionmentioning

confidence: 99%

Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases

Chatziioannou

Georgiadis

Hebels

et al. 2017

Sci Rep

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We recently reported that differential gene expression and DNA methylation profiles in blood leukocytes of apparently healthy smokers predicts with remarkable efficiency diseases and conditions known to be causally associated with smoking, suggesting that blood-based omic profiling of human populations may be useful for linking environmental exposures to potential health effects. Here we report on the sex-specific effects of tobacco smoking on transcriptomic and epigenetic features derived from genome-wide profiling in white blood cells, identifying 26 expression probes and 92 CpG sites, almost all of which are affected only in female smokers. Strikingly, these features relate to numerous genes with a key role in the pathogenesis of cardiovascular disease, especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as well as HMOX1 (haem oxygenase 1) and BCL2L1 (BCL2-like 1) which are involved in protection against oxidative stress and apoptosis, respectively. These results are in concordance with epidemiological evidence of higher female susceptibility to tobacco-induced cardiovascular disease and underline the potential of blood-based omic profiling in hazard and risk assessment.

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Section: Discussionmentioning

confidence: 99%

Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases

Chatziioannou

Georgiadis

Hebels

et al. 2017

Sci Rep

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“…31 PMPs play crucial roles in accelerating both atherosclerosis and thrombosis, as they possess various types of receptors and bioactive substances on their surface including GPIbα-IX-V, P-selectin, and integrins that can mediate platelet-monocyte/platelet-endotheliocyte interaction as well as T cell-mediated immune responses. 6,25,32 Therefore, controlling platelet apoptosis during the development of CVDs has been considered one of promising strategies for attenuating the progress of atherothrombosis. 31,33 Our present study demonstrated that PCA inhibited H 2 O 2 -induced platelet apoptosis in human platelets by modulating the expression of Bcl-2 family proteins and Cyto.…”

Section: Discussionmentioning

confidence: 99%

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Hong

et al. 2021

Thromb Haemost

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Oxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

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“…PL‐EVs may play a role in coagulation, immune function, and cell‐to‐cell communication . Circulating in patients with cardiovascular diseases, they become more important as players in pathogenesis and as biomarkers . In trauma patients, endogenous PL‐EVs negatively correlated with mortality and transfusion requirements .…”

Section: Discussionmentioning

confidence: 99%

Analysis of platelet‐derived extracellular vesicles in plateletpheresis concentrates: a multicenter study

et al. 2017

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Microparticles: A Novel Player in Cardiovascular Diseases

Cited by 3 publications

References 19 publications

Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases

Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Analysis of platelet‐derived extracellular vesicles in plateletpheresis concentrates: a multicenter study

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