Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms12727
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Funding
- Burroughs Wellcome Foundation
- Wellcome Trust [172805-01]
- Novartis foundation for medical-biological research
- NSF (USA)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, Brazil
- Novartis Foundation (Switzerland)
- American Heart Association
- Swiss National Science Foundation (Switzerland)
- Swedish Research Council (Sweden)
- Harvard Catalyst (NIH) [UL1 RR 025758]
- Harvard University and its affiliated academic health-care centres
- [NIH R01HL014006]
- [NIH 5R01AI091787]
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Malaria remains one of the greatest public health challenges worldwide, particularly in sub-Saharan Africa. The clinical outcome of individuals infected with Plasmodium falciparum parasites depends on many factors including host systemic inflammatory responses, parasite sequestration in tissues and vascular dysfunction. Production of pro-inflammatory cytokines and chemokines promotes endothelial activation as well as recruitment and infiltration of inflammatory cells, which in turn triggers further endothelial cell activation and parasite sequestration. Inflammatory responses are triggered in part by bioactive parasite products such as hemozoin and infected red blood cell-derived extracellular vesicles (iRBC-derived EVs). Here we demonstrate that such EVs contain functional miRNA-Argonaute 2 complexes that are derived from the host RBC. Moreover, we show that EVs are efficiently internalized by endothelial cells, where the miRNA-Argonaute 2 complexes modulate target gene expression and barrier properties. Altogether, these findings provide a mechanistic link between EVs and vascular dysfunction during malaria infection.
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