Schematic showing how P. falciparum acquires cholesterol from the external environment and stores it in the pRBC. First, the parasite takes up cholesterol (a lipoprotein component produced in the liver). Next, cholesterol as a part of the lipid membrane migrates in the cytosol of the pRBC, and/or also forms lipid membrane whorls for lipid/cholesterol storage. These membranes finally reach the parasite’s parasitophorous vacuole membrane from where cholesterol is imported into its body. The first step of this mechanism relates to the present study, but how the lipoprotein component passes through the pRBC membrane is currently unknown.
Hayakawa EH, Kato H, Nardone GA, Usukura J. A prospective mechanism and source of cholesterol uptake by Plasmodium falciparum-infected erythrocytes co-cultured with HepG2 cells. Parasitol Int. 2020 24:102179
Lower panel: Cholesterol gradient in erythrocytes infected with Plasmodium falciparum and localization of several putative cholesterol-binding or transport proteins. The level of cholesterol in each membrane – the erythrocyte plasma membrane (EPM), the parasitophorous membrane (PVM) and the parasite plasma membrane (PPM) – is indicated by the blue coloring. The EPM contains the highest concentration of cholesterol, followed by the PVM and then the PPM. PV-parasitophorous vacuole. Also indicated are the locations of several parasite proteins that are known or have been proposed to have a role in cholesterol transport.
Other associated proteins
|PF3D7_0107500||Niemann-Pick type c1-related protein|
|PF3D7_1426500||ABC transporter G family member 2|