Please use this identifier to cite or link to this item:
http://bura.brunel.ac.uk/handle/2438/20049
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DC Field | Value | Language |
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dc.contributor.author | Gomez, I | - |
dc.contributor.author | Ward, B | - |
dc.contributor.author | Souilhol, C | - |
dc.contributor.author | Recarti, C | - |
dc.contributor.author | Ariaans, M | - |
dc.contributor.author | Johnston, J | - |
dc.contributor.author | Burnett, A | - |
dc.contributor.author | Mahmoud, M | - |
dc.contributor.author | Luong, LA | - |
dc.contributor.author | West, L | - |
dc.contributor.author | Long, M | - |
dc.contributor.author | Parry, S | - |
dc.contributor.author | Woods, R | - |
dc.contributor.author | Hulston, C | - |
dc.contributor.author | Benedikter, B | - |
dc.contributor.author | Niespolo, C | - |
dc.contributor.author | Bazaz, R | - |
dc.contributor.author | Francis, S | - |
dc.contributor.author | Kiss-Toth, E | - |
dc.contributor.author | van Zandvoort, M | - |
dc.contributor.author | Schober, A | - |
dc.contributor.author | Hellewell, P | - |
dc.contributor.author | Evans, PC | - |
dc.contributor.author | Ridger, V | - |
dc.date.accessioned | 2020-01-20T15:10:54Z | - |
dc.date.available | 2020-12 | - |
dc.date.available | 2020-01-20T15:10:54Z | - |
dc.date.issued | 2020 | - |
dc.identifier | 214 | - |
dc.identifier | 214 | - |
dc.identifier.citation | Nature Communications, 2020, 11 (1) | en_US |
dc.identifier.issn | 214 | - |
dc.identifier.issn | 214 | - |
dc.identifier.issn | http://dx.doi.org/10.1038/s41467-019-14043-y | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | http://bura.brunel.ac.uk/handle/2438/20049 | - |
dc.description.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. | en_US |
dc.description.sponsorship | British Heart Foundation Programme Grant (CS, PE); British Heart Foundation Project Grants PG/09/067/27901 (AB, VR), PG/13/55/30365 (LW, SF), PG/14/38/30862 (CR, VR), PG/16/44/32146 (JJ, EKT, SF); British Heart Foundation Studentship FS/14/8/30605 (BW, VR); MRC Fellowship MR/K023977/1 (RB); and European Union’s Horizon 2020 Marie Skłodowska-Curie Innovative Training Network, TRAIN 721532 (CN). | en_US |
dc.language | en | - |
dc.language.iso | en | en_US |
dc.publisher | Springer Science and Business Media LLC | en_US |
dc.title | Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium | en_US |
dc.type | Article | en_US |
dc.identifier.doi | http://dx.doi.org/10.1038/s41467-019-14043-y | - |
dc.relation.isPartOf | Nature Communications | - |
pubs.issue | 1 | - |
pubs.publication-status | Published online | - |
pubs.volume | 11 | - |
dc.identifier.eissn | 2041-1723 | - |
Appears in Collections: | Dept of Life Sciences Research Papers |
Files in This Item:
File | Description | Size | Format | |
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FullText.pdf | 7.51 MB | Adobe PDF | View/Open |
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