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Updated: Jul 8, 2026
09:15
Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
Published on: January 21, 2020
Retinoic acid induced suicidal erythrocyte death
Olivier M Niemoeller1, Michael Foller, Camelia Lang
1Department of Physiology, University of Tuebingen, Tubingen, Germany.
Summary
Retinoic acid and TTNPB induce eryptosis, or suicidal erythrocyte death, by increasing phosphatidylserine exposure and cell shrinkage. This mechanism may enhance the clearance of malaria-parasitized red blood cells.
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Vitamin A and retinoic acid offer protection against severe malaria by promoting phagocytosis of infected erythrocytes.
- Phagocytosis of erythrocytes is linked to phosphatidylserine exposure on the cell surface.
Purpose of the Study:
- To investigate the effects of retinoic acid and the RAR agonist TTNPB on erythrocyte phosphatidylserine exposure.
- To determine if these retinoids induce eryptosis, a form of programmed cell death in erythrocytes.
Main Methods:
- Assessing annexin V binding to measure phosphatidylserine exposure on erythrocytes.
- Measuring erythrocyte forward scatter to detect cell shrinkage.
- Quantifying cytosolic Ca(2+)-activity using Fluo3 fluorescence.
- Evaluating the impact of Plasmodium falciparum infection on erythrocyte phosphatidylserine exposure.
Main Results:
- Retinoic acid and TTNPB significantly increased annexin V binding, indicating phosphatidylserine exposure.
- Both retinoids caused erythrocyte shrinkage, as shown by decreased forward scatter.
- Cytosolic Ca(2+)-activity was elevated by retinoic acid and TTNPB, a known trigger for phosphatidylserine exposure.
- TTNPB enhanced phosphatidylserine exposure in Plasmodium falciparum-infected erythrocytes.
Conclusions:
- Retinoic acid and TTNPB induce eryptosis, characterized by phosphatidylserine exposure and cell shrinkage.
- Eryptosis may contribute to the faster removal of malaria-parasitized erythrocytes from circulation after retinoid treatment.
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