Skip to main content
. 2017 Mar 21;8:474. doi: 10.3389/fmicb.2017.00474

FIGURE 1.

FIGURE 1

Human miRNAs response to Plasmodium falciparum infection. (A) Plasmodium-infected red blood cells (RBC). Translocation of miRNAs from RBC to P. falciparum inhibit translation of specific mRNAs of the parasite. (B) Transfer of miRNAs from Plasmodium-infected RBC to endothelial cells. Endocytosis by endothelial cell of EVs released by Plasmodium-infected RBC. miRNA-Argonaute 2 complexes alter gene expression and barrier properties in endothelial cells, contributing to malaria resistance. (C) Plasmodium-infected sickle cell erythrocyte. Translation inhibition of parasite mRNAs by sickle cell erythrocyte-miRNAs. miR-223, miR-451and let-7i inhibit parasite growth. Upward arrows denote an increase in expression of miR-451 and let-7i. EV, extracellular vesicle.