Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium

Ingrid Gomez, Ben Ward, Celine Souilhol, Chiara Recarti, Mark Ariaans, Jessica Johnston, Amanda Burnett, Marwa Mahmoud, Le Anh Luong, Laura West, Merete Long, Sion Parry, Rachel Woods, Carl Hulston, Birke Benedikter, Chiara Niespolo, Rohit Bazaz, Sheila Francis, Endre Kiss-Toth, Marc Zandvoort, Andreas Schober, Paul Hellewell, Paul C. Evans and Victoria Ridger ()
Additional contact information
Ingrid Gomez: University of Sheffield
Ben Ward: University of Sheffield
Celine Souilhol: University of Sheffield
Chiara Recarti: University of Sheffield
Mark Ariaans: University of Sheffield
Jessica Johnston: University of Sheffield
Amanda Burnett: University of Sheffield
Marwa Mahmoud: University of Sheffield
Le Anh Luong: Queen Mary University
Laura West: University of Sheffield
Merete Long: University of Sheffield
Sion Parry: Loughborough University
Rachel Woods: Loughborough University
Carl Hulston: Loughborough University
Birke Benedikter: Maastricht University
Chiara Niespolo: University of Sheffield
Rohit Bazaz: University of Sheffield
Sheila Francis: University of Sheffield
Endre Kiss-Toth: University of Sheffield
Marc Zandvoort: Maastricht University
Andreas Schober: Ludwig-Maximilian University of Munich
Paul Hellewell: University of Sheffield
Paul C. Evans: University of Sheffield
Victoria Ridger: University of Sheffield

Nature Communications, 2020, vol. 11, issue 1, 1-18

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-019-14043-y

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