ArticleCellular microbiology2017
Differential time-dependent volumetric and surface area changes and delayed induction of new permeation pathways in P. falciparum-infected hemoglobinopathic erythrocytes.
Article in Cellular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Rosette margination in blood flow during malaria pathogenesis.Biophysical journal · 2026Article
- Clathrins Are Involved in the Endocytosis of Host Cytosol in the Malaria Parasite.Traffic (Copenhagen, Denmark) · 2026Article
- Contact Dynamics of CytoadheringACS infectious diseases · 2025Article
- Deep learning image analysis for continuous single-cell imaging of dynamic processes in Plasmodium falciparum-infected erythrocytes.Communications biology · 2025Article
- Progeny counter mechanism in malaria parasites is linked to extracellular resources.PLoS pathogens · 2023Article
- pH-dependence of the Plasmodium falciparum chloroquine resistance transporter is linked to the transport cycle.Nature communications · 2023Article
- PfCRT mutations conferring piperaquine resistance in falciparum malaria shape the kinetics of quinoline drug binding and transport.PLoS pathogens · 2023Article
- The circulatory dynamics of human red blood cell homeostasis: Oxy-deoxy and PIEZO1-triggered changes.Biophysical journal · 2023Article
- The Knock-Down of the Chloroquine Resistance Transporter PfCRT Is Linked to Oligopeptide Handling in Plasmodium falciparum.Microbiology spectrum · 2022Article
- Biophysical Tools and Concepts Enable Understanding of Asexual Blood Stage Malaria.Frontiers in cellular and infection microbiology · 2022Review
- Impact of Sickle Cell Trait Hemoglobin on the Intraerythrocytic Transcriptional Program of Plasmodium falciparum.mSphere · 2021Article
- Functionalized supported membranes for quantifying adhesion of P. falciparum-infected erythrocytes.Biophysical journal · 2021Article
- Sickle-trait hemoglobin reduces adhesion to both CD36 and EPCR by Plasmodium falciparum-infected erythrocytes.PLoS pathogens · 2021Article
- Surface area-to-volume ratio, not cellular viscoelasticity, is the major determinant of red blood cell traversal through small channels.Cellular microbiology · 2021Article
- How Many Is Enough? - Challenges of Multinucleated Cell Division in Malaria Parasites.Frontiers in cellular and infection microbiology · 2021Review
- Cation-Chloride Cotransporters, Na/K Pump, and Channels in Cell Water and Ion Regulation:Frontiers in cell and developmental biology · 2021Article
- Article
- Born to sweet delight: Using natural models of malaria protection to understand and neutralize P. falciparum pathogenesis.PLoS pathogens · 2019Article
- Multimodal analysis of Plasmodium knowlesi-infected erythrocytes reveals large invaginations, swelling of the host cell, and rheological defects.Cellular microbiology · 2019Article
- Hemoglobin S and C affect biomechanical membrane properties ofCommunications biology · 2019Article
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9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
During intraerythrocytic development, Plasmodium falciparum increases the ion permeability of the erythrocyte plasma membrane to an extent that jeopardizes the osmotic stability of the host cell. A previously formulated numeric model has suggested that the parasite prevents premature rupture of the host cell by consuming hemoglobin (Hb) in excess of its own anabolic needs. Here, we have tested the colloid-osmotic model on the grounds of time-resolved experimental measurements on cell surface area and volume. We have further verified whether the colloid-osmotic model can predict time-dependent volumetric changes when parasites are grown in erythrocytes containing the hemoglobin variants S or C. A good agreement between model-predicted and empirical data on both infected erythrocyte and intracellular parasite volume was found for parasitized HbAA and HbAC erythrocytes. However, a delayed induction of the new permeation pathways needed to be taken into consideration for the latter case. For parasitized HbAS erythrocyte, volumes diverged from model predictions, and infected erythrocytes showed excessive vesiculation during the replication cycle. We conclude that the colloid-osmotic model provides a plausible and experimentally supported explanation of the volume expansion and osmotic stability of P. falciparum-infected erythrocytes. The contribution of vesiculation to the malaria-protective function of hemoglobin S is discussed.
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