Bilberry Supplementation after Myocardial Infarction Decreases Microvesicles in Blood and Affects Endothelial Vesiculation.
Aged
Blood Platelets
/ cytology
Blood Proteins
/ metabolism
Cell-Derived Microparticles
/ drug effects
Dietary Supplements
Endothelial Cells
/ drug effects
Extracellular Vesicles
Female
Gene Expression
Hematologic Tests
/ methods
Human Umbilical Vein Endothelial Cells
Humans
Male
Myocardial Infarction
/ blood
Nanoparticles
Phosphorylation
/ drug effects
Receptors, Purinergic P2X7
/ genetics
Vaccinium myrtillus
P2X7 (P2X purinoreceptor 7)
bilberries
cardiovascular diseases
microvesicles
Journal
Molecular nutrition & food research
ISSN: 1613-4133
Titre abrégé: Mol Nutr Food Res
Pays: Germany
ID NLM: 101231818
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
04
02
2020
revised:
02
07
2020
pubmed:
28
8
2020
medline:
3
8
2021
entrez:
27
8
2020
Statut:
ppublish
Résumé
Diet rich in bilberries is considered cardioprotective, but the mechanisms of action are poorly understood. Cardiovascular disease is characterized by increased proatherogenic status and high levels of circulating microvesicles (MVs). In an open-label study patients with myocardial infarction receive an 8 week dietary supplementation with bilberry extract (BE). The effect of BE on patient MV levels and its influence on endothelial vesiculation in vitro is investigated. MVs are captured with acoustic trapping and platelet-derived MVs (PMVs), as well as endothelial-derived MVs (EMVs) are quantified with flow cytometry. The in vitro effect of BE on endothelial extracellular vesicle (EV) release is examined using endothelial cells and calcein staining. The mechanisms of BE influence on vesiculation pathways are studied by Western blot and qRT-PCR. Supplementation with BE decreased both PMVs and EMVs. Furthermore, BE reduced endothelial EV release, Akt phosphorylation, and vesiculation-related gene transcription. It also protects the cells from P2X BE supplementation improves the MV profile in patient blood and reduces endothelial vesiculation through several molecular mechanisms related to the P2X
Identifiants
pubmed: 32846041
doi: 10.1002/mnfr.202000108
pmc: PMC7685140
doi:
Substances chimiques
Blood Proteins
0
P2RX7 protein, human
0
Receptors, Purinergic P2X7
0
Types de publication
Journal Article
Pragmatic Clinical Trial
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2000108Informations de copyright
© 2020 The Authors. Published by Wiley-VCH GmbH.
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