Infected erythrocyte-derived extracellular vesicles alter vascular function via regulatory Ago2-miRNA complexes in malaria

Pierre-Yves Mantel (), Daisy Hjelmqvist, Michael Walch, Solange Kharoubi-Hess, Sandra Nilsson, Deepali Ravel, Marina Ribeiro, Christof Grüring, Siyuan Ma, Prasad Padmanabhan, Alexander Trachtenberg, Johan Ankarklev, Nicolas M. Brancucci, Curtis Huttenhower, Manoj T. Duraisingh, Ionita Ghiran, Winston P. Kuo, Luis Filgueira, Roberta Martinelli and Matthias Marti ()
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Pierre-Yves Mantel: Harvard T.H. Chan School of Public Health
Daisy Hjelmqvist: Harvard T.H. Chan School of Public Health
Michael Walch: Unit of Anatomy, University of Fribourg
Solange Kharoubi-Hess: Unit of Anatomy, University of Fribourg
Sandra Nilsson: Harvard T.H. Chan School of Public Health
Deepali Ravel: Harvard T.H. Chan School of Public Health
Marina Ribeiro: Harvard T.H. Chan School of Public Health
Christof Grüring: Harvard T.H. Chan School of Public Health
Siyuan Ma: Harvard T.H. Chan School of Public Health
Prasad Padmanabhan: Harvard T.H. Chan School of Public Health
Alexander Trachtenberg: Harvard Catalyst Laboratory for Innovative Translational Technologies, Harvard Medical School
Johan Ankarklev: Harvard T.H. Chan School of Public Health
Nicolas M. Brancucci: Harvard T.H. Chan School of Public Health
Curtis Huttenhower: Harvard T.H. Chan School of Public Health
Manoj T. Duraisingh: Harvard T.H. Chan School of Public Health
Ionita Ghiran: Beth Israel Deaconess Medical Center
Winston P. Kuo: Harvard Catalyst Laboratory for Innovative Translational Technologies, Harvard Medical School
Luis Filgueira: Unit of Anatomy, University of Fribourg
Roberta Martinelli: Center for Vascular Biology Research, Beth Israel Deaconess Medical Center
Matthias Marti: Harvard T.H. Chan School of Public Health

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms12727

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