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Updated: Feb 3, 2026
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Dysfunctional endothelial-derived microparticles promote inflammatory macrophage formation via NF-кB and IL-1β signal
Yanfang Wang1, Jie Liu1, Xiaoli Chen1
1Key Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
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.
Insights
Endothelial-derived microparticles (EMPs) from dysfunctional cells increase in acute coronary syndrome (ACS). These EMPs promote inflammation and monocyte activation, suggesting EMPs as a therapeutic target in ACS.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Circulating endothelial-derived microparticles (EMPs) are elevated in acute coronary syndrome (ACS).
- The specific role and underlying mechanisms of EMPs from dysfunctional endothelium in ACS pathogenesis remain unclear.
Purpose of the Study:
- To investigate the role of EMPs from dysfunctional endothelium in ACS.
- To elucidate the mechanisms by which EMPs influence monocyte activation and inflammatory responses.
Main Methods:
- Plasma EMP levels were quantified in ACS patients and controls.
- EMPs from stressed and healthy human umbilical vein endothelial cells (HUVECs) were compared.
- Monocyte incorporation of EMPs, NF-κB translocation, and inflammatory cytokine production were analyzed.
Main Results:
- ACS patients exhibited significantly higher plasma EMP levels than controls.
- EMPs from stressed HUVECs were incorporated into monocytes and induced pro-inflammatory cytokine release via NF-κB and IL-1β pathways.
- Dysfunctional EMPs promoted monocyte adhesion, proliferation, and foam cell formation, indicating enhanced inflammatory potential.
Conclusions:
- EMPs from dysfunctional endothelium contribute to the inflammatory process in ACS.
- NF-κB and IL-1β signaling pathways are critical mediators of EMP-induced inflammation in ACS.
- Targeting EMP-mediated inflammatory responses presents a potential therapeutic strategy for ACS.
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