Bubble-Induced Endothelial Microparticles Promote Endothelial Dysfunction

Decompression sickness is a systemic pathophysiological process caused by bubbles and endothelial microparticles (EMPs) are established markers reflecting competency of endothelial function and vascular biology. Here, we investigated the effects of bubble-induced EMPs on endothelial cells in vitro a...

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Bibliographic Details
Published in:PloS one 2017-01, Vol.12 (1), p.e0168881-e0168881
Main Authors: Yu, Xuhua, Xu, Jiajun, Huang, Guoyang, Zhang, Kun, Qing, Long, Liu, Wenwu, Xu, Weigang
Format: Article
Language:English
Subjects:
Adhesion
Adhesion tests
Animals
Annexin V
Apoptosis
Biological effects
Biology and Life Sciences
Bubble effects
Bubbles
Cell adhesion
Cell permeability
Cell-Derived Microparticles
Cells, Cultured
Cytokines
Decompression
Decompression sickness
Development and progression
Endothelial cells
Endothelium
Endothelium, Vascular - physiopathology
Enzyme-linked immunosorbent assay
Hypertension
In vivo methods and tests
Inflammation
Injuries
Intercellular adhesion molecule 1
Intracellular
Intravenous administration
Laboratory animals
Male
Medicine
Medicine and Health Sciences
Microparticles
Microvasculature
Nanoparticles
Neutrophils
Nitric oxide
Overexpression
Oxygen
Permeability
Physiology
Rats
Rats, Sprague-Dawley
Reactive oxygen species
Research and Analysis Methods
Rodents
Studies
Substrates
Thrombomodulin
Thrombosis
Tumor necrosis factor-TNF
Vascular diseases
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Summary:Decompression sickness is a systemic pathophysiological process caused by bubbles and endothelial microparticles (EMPs) are established markers reflecting competency of endothelial function and vascular biology. Here, we investigated the effects of bubble-induced EMPs on endothelial cells in vitro and vivo. Rat pulmonary microvascular endothelial cells (PMVECs) were isolated and stimulated by bubbles and bubble-induced EMPs were collected and incubated with normal PMVECs in vitro. Cell viability and apoptosis were detected using Cell Counting Kit-8 assay and Annexin V FITC/PI double staining, respectively. Cell permeability and pro-inflammatory cytokines were determined by electric cell substrate impedance sensing and enzyme-linked immunosorbent assay, respectively. Intracellular nitric oxide and reactive oxygen species production were analyzed microscopically. In vivo study, bubble-induced EMPs were intravenously injected to the rats and soluble thrombomodulin, intercellular adhesion molecule 1, and vascullar adhesion molecule 1 were involved in evaluating endothelial dysfunction. In our study, bubble stimulus resulted in a significant increase of EMPs release by 3 fold. Bubble-induced EMPs significantly decreased cell viability and increased cell apoptosis. Moreover, bubble-induced EMPs induced abnormal increase of cell permeability and over-expression of pro-inflammatory cytokines. Intracellular ROS production increased while NO production decreased. These negative effects caused by bubble-induced EMPs were remarkably suppressed when EMPs pretreated with surfactant FSN-100. Finally, intravenous injection of bubble-induced EMPs caused elevations of soluble thrombomodulin and pro-inflammatory cytokines in the circulation. Altogether, our results demonstrated that bubble-induced EMPs can mediate endothelial dysfunction in vitro and vivo, which can be attenuated by EMPs abatement strategy. These data expanded our horizon of the detrimental effects of bubble-induced EMPs, which may be of great concern in DCS.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0168881