Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways

Yanfang Wang, Jie Liu, Xiaoli Chen, Huimin Sun, Sheng Peng, Yashu Kuang, Jingjiang Pi, Tao Zhuang, Lin Zhang, Zuoren Yu, Brain Tomlinson, Paul Chan, Yihan Chen, Yuzhen Zhang, Ying Li

研究成果: 雜誌貢獻文章

摘要

Background: Circulating endothelial-derived microparticles (EMPs) are reported to be increased in acute coronary syndrome (ACS). However, it remains unclear whether EMPs from dysfunctional endothelium participate in the initiation and progression of ACS and what the underlying mechanisms might be. Methods: Plasma EMPs were measured in 22 patients with ACS and 20 control patients without coronary artery diseases. EMPs from dysfunctional human umbilical vein endothelial cells (HUVECs) stressed by serum-starvation or hypoxia were compared to the EMPs from healthy HUVECs. Confocal and fluorescent microscopy was used to visualize the incorporation of EMPs into monocytes and the translocation of NF-кB. Monocyte adhesion, cell proliferation, and phagocytosis were detected by PKH26 red fluorescent labelling, Ki67 immunostaining, and Sudan IV staining for uptake of oxidized low-density lipoprotein, respectively. Results: Plasma EMPs was significantly increased in ACS patients compared to controls. EMPs were incorporated into monocytes and EMPs from stressed HUVECs produced more pro-inflammatory cytokines compared to vehicle control, which was depended on NF-кB and IL-1β signal pathways. EMPs from dysfunctional endothelium promoted monocyte adherence via NF-кB and IL-1β-mediated MCP-1 and CCR-5 signals, as well as proliferation via the NF-кB and IL-1β-mediated Cyclin D1 signals. Finally, EMPs from dysfunctional endothelium showed greater promotion of macrophage phagocytosis forming foam cells to produce more pro-inflammatory cytokines. Conclusion: MPs might be involved in the inflammatory process in patients with ACS via NF-κB and IL-1β-dependent signals. Targeting EMP-mediated inflammatory responses may be a promising therapeutic strategy to limit the progression of disease in ACS.
原文英語
頁(從 - 到)476-486
頁數11
期刊Journal of Cellular and Molecular Medicine
23
發行號1
DOIs
出版狀態已發佈 - 一月 1 2019

指紋

Acute Coronary Syndrome
Interleukin-1
Signal Transduction
Macrophages
Monocytes
Human Umbilical Vein Endothelial Cells
Endothelium
Cytokines
Cytophagocytosis
Foam Cells
Cyclin D1
Starvation
Phagocytosis
Confocal Microscopy
Disease Progression
Coronary Artery Disease
Cell Proliferation
Staining and Labeling
Serum

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology

引用此文

Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways. / Wang, Yanfang; Liu, Jie; Chen, Xiaoli; Sun, Huimin; Peng, Sheng; Kuang, Yashu; Pi, Jingjiang; Zhuang, Tao; Zhang, Lin; Yu, Zuoren; Tomlinson, Brain; Chan, Paul; Chen, Yihan; Zhang, Yuzhen; Li, Ying.

於: Journal of Cellular and Molecular Medicine, 卷 23, 編號 1, 01.01.2019, p. 476-486.

研究成果: 雜誌貢獻文章

Wang, Y, Liu, J, Chen, X, Sun, H, Peng, S, Kuang, Y, Pi, J, Zhuang, T, Zhang, L, Yu, Z, Tomlinson, B, Chan, P, Chen, Y, Zhang, Y & Li, Y 2019, 'Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways', Journal of Cellular and Molecular Medicine, 卷 23, 編號 1, 頁 476-486. https://doi.org/10.1111/jcmm.13950
Wang, Yanfang ; Liu, Jie ; Chen, Xiaoli ; Sun, Huimin ; Peng, Sheng ; Kuang, Yashu ; Pi, Jingjiang ; Zhuang, Tao ; Zhang, Lin ; Yu, Zuoren ; Tomlinson, Brain ; Chan, Paul ; Chen, Yihan ; Zhang, Yuzhen ; Li, Ying. / Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways. 於: Journal of Cellular and Molecular Medicine. 2019 ; 卷 23, 編號 1. 頁 476-486.
@article{19da0ca65cc54c61a85b1176ace6e636,
title = "Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways",
abstract = "Background: Circulating endothelial-derived microparticles (EMPs) are reported to be increased in acute coronary syndrome (ACS). However, it remains unclear whether EMPs from dysfunctional endothelium participate in the initiation and progression of ACS and what the underlying mechanisms might be. Methods: Plasma EMPs were measured in 22 patients with ACS and 20 control patients without coronary artery diseases. EMPs from dysfunctional human umbilical vein endothelial cells (HUVECs) stressed by serum-starvation or hypoxia were compared to the EMPs from healthy HUVECs. Confocal and fluorescent microscopy was used to visualize the incorporation of EMPs into monocytes and the translocation of NF-кB. Monocyte adhesion, cell proliferation, and phagocytosis were detected by PKH26 red fluorescent labelling, Ki67 immunostaining, and Sudan IV staining for uptake of oxidized low-density lipoprotein, respectively. Results: Plasma EMPs was significantly increased in ACS patients compared to controls. EMPs were incorporated into monocytes and EMPs from stressed HUVECs produced more pro-inflammatory cytokines compared to vehicle control, which was depended on NF-кB and IL-1β signal pathways. EMPs from dysfunctional endothelium promoted monocyte adherence via NF-кB and IL-1β-mediated MCP-1 and CCR-5 signals, as well as proliferation via the NF-кB and IL-1β-mediated Cyclin D1 signals. Finally, EMPs from dysfunctional endothelium showed greater promotion of macrophage phagocytosis forming foam cells to produce more pro-inflammatory cytokines. Conclusion: MPs might be involved in the inflammatory process in patients with ACS via NF-κB and IL-1β-dependent signals. Targeting EMP-mediated inflammatory responses may be a promising therapeutic strategy to limit the progression of disease in ACS.",
keywords = "acute coronary syndrome, endothelial microparticles, interleukin-1beta, NF-kappa B, vascular inflammation",
author = "Yanfang Wang and Jie Liu and Xiaoli Chen and Huimin Sun and Sheng Peng and Yashu Kuang and Jingjiang Pi and Tao Zhuang and Lin Zhang and Zuoren Yu and Brain Tomlinson and Paul Chan and Yihan Chen and Yuzhen Zhang and Ying Li",
year = "2019",
month = "1",
day = "1",
doi = "10.1111/jcmm.13950",
language = "English",
volume = "23",
pages = "476--486",
journal = "Journal of Cellular and Molecular Medicine",
issn = "1582-1838",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal pathways

AU - Wang, Yanfang

AU - Liu, Jie

AU - Chen, Xiaoli

AU - Sun, Huimin

AU - Peng, Sheng

AU - Kuang, Yashu

AU - Pi, Jingjiang

AU - Zhuang, Tao

AU - Zhang, Lin

AU - Yu, Zuoren

AU - Tomlinson, Brain

AU - Chan, Paul

AU - Chen, Yihan

AU - Zhang, Yuzhen

AU - Li, Ying

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Background: Circulating endothelial-derived microparticles (EMPs) are reported to be increased in acute coronary syndrome (ACS). However, it remains unclear whether EMPs from dysfunctional endothelium participate in the initiation and progression of ACS and what the underlying mechanisms might be. Methods: Plasma EMPs were measured in 22 patients with ACS and 20 control patients without coronary artery diseases. EMPs from dysfunctional human umbilical vein endothelial cells (HUVECs) stressed by serum-starvation or hypoxia were compared to the EMPs from healthy HUVECs. Confocal and fluorescent microscopy was used to visualize the incorporation of EMPs into monocytes and the translocation of NF-кB. Monocyte adhesion, cell proliferation, and phagocytosis were detected by PKH26 red fluorescent labelling, Ki67 immunostaining, and Sudan IV staining for uptake of oxidized low-density lipoprotein, respectively. Results: Plasma EMPs was significantly increased in ACS patients compared to controls. EMPs were incorporated into monocytes and EMPs from stressed HUVECs produced more pro-inflammatory cytokines compared to vehicle control, which was depended on NF-кB and IL-1β signal pathways. EMPs from dysfunctional endothelium promoted monocyte adherence via NF-кB and IL-1β-mediated MCP-1 and CCR-5 signals, as well as proliferation via the NF-кB and IL-1β-mediated Cyclin D1 signals. Finally, EMPs from dysfunctional endothelium showed greater promotion of macrophage phagocytosis forming foam cells to produce more pro-inflammatory cytokines. Conclusion: MPs might be involved in the inflammatory process in patients with ACS via NF-κB and IL-1β-dependent signals. Targeting EMP-mediated inflammatory responses may be a promising therapeutic strategy to limit the progression of disease in ACS.

AB - Background: Circulating endothelial-derived microparticles (EMPs) are reported to be increased in acute coronary syndrome (ACS). However, it remains unclear whether EMPs from dysfunctional endothelium participate in the initiation and progression of ACS and what the underlying mechanisms might be. Methods: Plasma EMPs were measured in 22 patients with ACS and 20 control patients without coronary artery diseases. EMPs from dysfunctional human umbilical vein endothelial cells (HUVECs) stressed by serum-starvation or hypoxia were compared to the EMPs from healthy HUVECs. Confocal and fluorescent microscopy was used to visualize the incorporation of EMPs into monocytes and the translocation of NF-кB. Monocyte adhesion, cell proliferation, and phagocytosis were detected by PKH26 red fluorescent labelling, Ki67 immunostaining, and Sudan IV staining for uptake of oxidized low-density lipoprotein, respectively. Results: Plasma EMPs was significantly increased in ACS patients compared to controls. EMPs were incorporated into monocytes and EMPs from stressed HUVECs produced more pro-inflammatory cytokines compared to vehicle control, which was depended on NF-кB and IL-1β signal pathways. EMPs from dysfunctional endothelium promoted monocyte adherence via NF-кB and IL-1β-mediated MCP-1 and CCR-5 signals, as well as proliferation via the NF-кB and IL-1β-mediated Cyclin D1 signals. Finally, EMPs from dysfunctional endothelium showed greater promotion of macrophage phagocytosis forming foam cells to produce more pro-inflammatory cytokines. Conclusion: MPs might be involved in the inflammatory process in patients with ACS via NF-κB and IL-1β-dependent signals. Targeting EMP-mediated inflammatory responses may be a promising therapeutic strategy to limit the progression of disease in ACS.

KW - acute coronary syndrome

KW - endothelial microparticles

KW - interleukin-1beta

KW - NF-kappa B

KW - vascular inflammation

UR - http://www.scopus.com/inward/record.url?scp=85055136263&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85055136263&partnerID=8YFLogxK

U2 - 10.1111/jcmm.13950

DO - 10.1111/jcmm.13950

M3 - Article

C2 - 30334371

AN - SCOPUS:85055136263

VL - 23

SP - 476

EP - 486

JO - Journal of Cellular and Molecular Medicine

JF - Journal of Cellular and Molecular Medicine

SN - 1582-1838

IS - 1

ER -