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Updated: Jun 12, 2026
09:15
Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
Published on: January 21, 2020
Monensin induced suicidal erythrocyte death
Shefalee K Bhavsar1, Matthias Eberhard, Diwakar Bobbala
1Department of Physiology, University of Tübingen, 72076 Tübingen, Germany.
Summary
Monensin, a sodium ionophore, triggers suicidal erythrocyte death (eryptosis) by increasing cytosolic calcium and causing cell membrane scrambling. This study reveals monensin dissociates cell volume changes from membrane alterations during eryptosis.
Area of Science:
- Hematology
- Cell Biology
- Physiology
Background:
- Eryptosis, or suicidal erythrocyte death, involves cell membrane scrambling and shrinkage.
- Triggers include hyperosmotic stress, ionophore-induced ion flux, and energy depletion.
- Increased cytosolic calcium (Ca2+) is a key factor in eryptosis.
Purpose of the Study:
- To investigate the effect of the sodium ionophore monensin on erythrocyte cell volume and eryptosis.
- To determine if monensin influences the dissociation of cell membrane alterations and cell volume changes during eryptosis.
Main Methods:
- Eryptosis was induced using monensin and glucose depletion.
- Cell membrane scrambling was assessed via annexin V binding to phosphatidylserine.
- Cell volume was measured by forward scatter in flow cytometry.
- Cytosolic Ca2+ and ATP concentrations were quantified using fluorescence and luminescence assays, respectively.
Main Results:
- Monensin exposure increased forward scatter, cytosolic Ca2+, and annexin V binding.
- Glucose depletion decreased forward scatter but increased cytosolic Ca2+ and annexin V binding.
- Monensin partially reversed the volume changes induced by glucose depletion while augmenting Ca2+ and annexin V increases.
Conclusions:
- Monensin induces eryptosis independently of significant cell shrinkage.
- Monensin treatment dissociates cell membrane scrambling from cell volume changes in suicidal erythrocyte death.
- These findings highlight a novel mechanism in eryptosis regulation.
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