Calciprotein Particles Cause Endothelial Dysfunction under Flow

Calciprotein particles (CPPs), which increasingly arise in the circulation during the disorders of mineral homeostasis, represent a double-edged sword protecting the human organism from extraskeletal calcification but potentially causing endothelial dysfunction. Existing models, however, failed to d...

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Veröffentlicht in:International journal of molecular sciences 2020-11, Vol.21 (22), p.8802
Hauptverfasser: Shishkova, Daria, Markova, Victoria, Sinitsky, Maxim, Tsepokina, Anna, Velikanova, Elena, Bogdanov, Leo, Glushkova, Tatiana, Kutikhin, Anton
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container_issue 22
container_start_page 8802
container_title International journal of molecular sciences
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creator Shishkova, Daria
Markova, Victoria
Sinitsky, Maxim
Tsepokina, Anna
Velikanova, Elena
Bogdanov, Leo
Glushkova, Tatiana
Kutikhin, Anton
description Calciprotein particles (CPPs), which increasingly arise in the circulation during the disorders of mineral homeostasis, represent a double-edged sword protecting the human organism from extraskeletal calcification but potentially causing endothelial dysfunction. Existing models, however, failed to demonstrate the detrimental action of CPPs on endothelial cells (ECs) under flow. Here, we applied a flow culture system, where human arterial ECs were co-incubated with CPPs for 4 h, and a normolipidemic and normotensive rat model (10 daily intravenous injections of CPPs) to simulate the scenario occurring in vivo in the absence of confounding cardiovascular risk factors. Pathogenic effects of CPPs were investigated by RT-qPCR and Western blotting profiling of the endothelial lysate. CPPs were internalised within 1 h of circulation, inducing adhesion of peripheral blood mononuclear cells to ECs. Molecular profiling revealed that CPPs stimulated the expression of pro-inflammatory cell adhesion molecules VCAM1 and ICAM1 and upregulated transcription factors of endothelial-to-mesenchymal transition (Snail, Slug and Twist1). Furthermore, exposure to CPPs reduced the production of atheroprotective transcription factors KLF2 and KLF4 and led to YAP1 hypophosphorylation, potentially disturbing the mechanisms responsible for the proper endothelial mechanotransduction. Taken together, our results suggest the ability of CPPs to initiate endothelial dysfunction at physiological flow conditions.
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source MEDLINE; MDPI - Multidisciplinary Digital Publishing Institute; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Animals
Blood circulation
Calcification
Calcifying Nanoparticles - adverse effects
Calcium - chemistry
Cardiovascular diseases
Cell adhesion
Cell adhesion & migration
Cell adhesion molecules
Cell culture
Cells, Cultured
Coronary vessels
Cytokines
Endothelial cells
Endothelial Cells - pathology
Gene expression
Homeostasis
Humans
Inflammation
Intercellular adhesion molecule 1
Intravenous administration
Investigations
KLF4 protein
Krueppel-like factor
Leukocytes (mononuclear)
Male
Mechanotransduction
Mechanotransduction, Cellular
Mesenchyme
Peripheral blood mononuclear cells
Rats
Rats, Wistar
Risk analysis
Risk factors
Smooth muscle
Snail protein
Stress, Mechanical
Transcription factors
Vascular Diseases - metabolism
Veins & arteries
Western blotting
Yes-associated protein
title Calciprotein Particles Cause Endothelial Dysfunction under Flow
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