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On-Chip Endothelial Inflammatory Phenotyping
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Endothelial extracellular vesicles modulate the macrophage phenotype: Potential implications in atherosclerosis
1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Scandinavian Journal of Immunology
|February 22, 2018
Summary
Extracellular vesicles (EVs) from endothelial cells influence monocyte/macrophage behavior. EVs from oxidized LDL-treated cells promote inflammation, while those from KLF2-transduced cells reduce it, impacting atherosclerosis development.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Immunology
Background:
- Endothelial cells (ECs) and macrophages interact critically in cardiovascular health and atherosclerosis.
- Extracellular vesicles (EVs) mediate intercellular communication, but their role in EC-macrophage interactions during atherosclerosis is unclear.
- Oxidized low-density lipoprotein (ox-LDL) and Kruppel-like factor 2 (KLF2) influence ECs, potentially altering EV cargo and function.
Purpose of the Study:
- To investigate the impact of EVs from ox-LDL-treated and/or KLF2-transduced ECs on monocyte/macrophage phenotype.
- To determine the role of microRNA-155 (miR-155) in mediating these EV effects.
- To assess the therapeutic potential of EC-derived EVs in an in vivo model of atherosclerosis.
Main Methods:
- Quantitative PCR (Q-PCR) to measure miR-155 expression in human umbilical vein endothelial cells (HUVECs).
- Co-culture systems, immunofluorescence, and flow cytometry to analyze EV transfer and monocyte/macrophage polarization.
- In vivo studies using mouse models with oil red staining to evaluate atherosclerotic lesions.
Main Results:
- Both ox-LDL and KLF2 modulated miR-155 expression in HUVECs.
- EVs from ox-LDL-treated ECs transferred miR-155 to monocytes, promoting a pro-inflammatory M1 macrophage phenotype.
- EVs from KLF2-expressing ECs suppressed monocyte activation and reduced atherosclerotic lesions in mice, associated with decreased miR-155.
- KLF2-EVs shifted macrophage balance towards anti-inflammatory M2 phenotypes.
Conclusions:
- EVs secreted by ECs, particularly their microRNA content, significantly influence monocyte/macrophage activation.
- miR-155 plays a key role in mediating the pro-atherogenic effects of EVs from ox-LDL-exposed ECs.
- KLF2-modified EC-derived EVs exhibit anti-atherogenic properties, offering potential therapeutic strategies for cardiovascular disease.
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