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Updated: Dec 31, 2025
Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
Published on: August 12, 2025
Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium
Ingrid Gomez1, Ben Ward1,2, Celine Souilhol1,2
1Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Abstract:
Neutrophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels of circulating neutrophil microvesicles are enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulate at disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesicles promote inflammatory gene expression by delivering miR-155, enhancing NF-κB activation. Similarly, neutrophil microvesicles increase miR-155 and enhance NF-κB at disease-prone sites of disturbed flow in vivo. Enhancement of atherosclerotic plaque formation and increase in macrophage content by neutrophil microvesicles is dependent on miR-155. We conclude that neutrophils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying miR-155 to disease-prone regions.
Insights
Neutrophil microvesicles, elevated by high-fat diets, promote atherosclerosis. These microvesicles deliver miR-155, driving vascular inflammation and plaque formation in arteries.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Neutrophils play a role in atherosclerosis pathogenesis but are rarely found in plaques.
- The specific contribution of neutrophil-derived microvesicles to arterial disease remains unclear.
Purpose of the Study:
- To investigate the role of neutrophil-derived microvesicles in arterial pathophysiology.
- To determine if neutrophil microvesicles influence vascular inflammation and atherosclerosis.
Main Methods:
- Assessed circulating neutrophil microvesicle levels in mice on a high-fat diet.
- Examined microvesicle accumulation in arteries under disturbed flow conditions.
- Utilized cultured endothelial cells and a murine model to study microvesicle effects on inflammation and atherosclerosis, including miR-155 and NF-κB activation.
Main Results:
- High-fat diet increased circulating neutrophil microvesicle levels.
- Neutrophil microvesicles accumulated in arteries prone to disturbed flow.
- Microvesicles promoted vascular inflammation and atherosclerosis in mice, dependent on miR-155.
- Neutrophil microvesicles delivered miR-155 to endothelial cells, enhancing NF-κB activation and inflammatory gene expression.
Conclusions:
- Neutrophil-derived microvesicles contribute to vascular inflammation and atherosclerosis.
- Microvesicles act by delivering miR-155 to disease-prone arterial regions, activating NF-κB.
- Neutrophils are implicated in atherogenesis via microvesicle-mediated miR-155 transfer.
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