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Endothelial cells suppress monocyte activation through secretion of extracellular vesicles containing antiinflammatory microRNAs

Blood, 2015-05, Vol.125 (20), p.3202-3212 [Peer Reviewed Journal]

2015 American Society of Hematology ;2015 by The American Society of Hematology. ;2015 by The American Society of Hematology 2015 ;ISSN: 0006-4971 ;ISSN: 1528-0020 ;EISSN: 1528-0020 ;DOI: 10.1182/blood-2014-11-611046 ;PMID: 25838349

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Title:
Endothelial cells suppress monocyte activation through secretion of extracellular vesicles containing antiinflammatory microRNAs
Author: Njock, Makon-Sébastien ; Cheng, Henry S. ; Dang, Lan T. ; Nazari-Jahantigh, Maliheh ; Lau, Andrew C. ; Boudreau, Emilie ; Roufaiel, Mark ; Cybulsky, Myron I. ; Schober, Andreas ; Fish, Jason E.
Subjects: Cardiovascular & respiratory systems ; Cell Communication ; Cell Line ; Coculture Techniques ; Endothelial Cells - metabolism ; Extracellular Space ; Human health sciences ; Humans ; Inflammation - genetics ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation/genetics/immunology/metabolism ; Interferon Regulatory Factors - metabolism ; Lipopolysaccharides - immunology ; MicroRNAs - genetics ; Monocytes - immunology ; Monocytes - metabolism ; Monocytes/immunology/metabolism ; NF-kappa B - metabolism ; Sciences de la santé humaine ; Secretory Vesicles - metabolism ; Signal Transduction ; Systèmes cardiovasculaire & respiratoire ; Vascular Biology
Is Part Of: Blood, 2015-05, Vol.125 (20), p.3202-3212
Description: The blood contains high concentrations of circulating extracellular vesicles (EVs), and their levels and contents are altered in several disease states, including cardiovascular disease. However, the function of circulating EVs, especially the microRNAs (miRNAs) that they contain, are poorly understood. We sought to determine the effect of secreted vesicles produced by quiescent endothelial cells (ECs) on monocyte inflammatory responses and to assess whether transfer of microRNAs occurs between these cells. We observed that monocytic cells cocultured (but not in contact) with ECs were refractory to inflammatory activation. Further characterization revealed that endothelium-derived EVs (EC-EVs) suppressed monocyte activation by enhancing immunomodulatory responses and diminishing proinflammatory responses. EVs isolated from mouse plasma also suppressed monocyte activation. Importantly, injection of EC-EVs in vivo repressed monocyte/macrophage activation, confirming our in vitro findings. We found that several antiinflammatory microRNAs were elevated in EC-EV–treated monocytes. In particular, miR-10a was transferred to monocytic cells from EC-EVs and could repress inflammatory signaling through the targeting of several components of the NF-κB pathway, including IRAK4. Our findings reveal that ECs secrete EVs that can modulate monocyte activation and suggest that altered EV secretion and/or microRNA content may affect vascular inflammation in the setting of cardiovascular disease. •Quiescent endothelial cells secrete extracellular vesicles that can be taken up by monocytes to suppress their activation.•MiR-10a is transferred to monocytic cells and inhibits the activation of the proinflammatory nuclear factor κB pathway.
Publisher: United States: Elsevier Inc
Language: English
Identifier: ISSN: 0006-4971
ISSN: 1528-0020
EISSN: 1528-0020
DOI: 10.1182/blood-2014-11-611046
PMID: 25838349
Source: GFMER Free Medical Journals
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Endothelial cells suppress monocyte activation through secretion of extracellular vesicles containing antiinflammatory microRNAs

2015 American Society of Hematology ;2015 by The American Society of Hematology. ;2015 by The American Society of Hematology 2015 ;ISSN: 0006-4971 ;ISSN: 1528-0020 ;EISSN: 1528-0020 ;DOI: 10.1182/blood-2014-11-611046 ;PMID: 25838349

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