Eryptosis triggered by bismuth |
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Authors: | Manuel Braun Michael Föller Erich Gulbins Florian Lang |
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Institution: | 1. Department of Physiology, University of Tübingen, Tübingen, Germany 2. Department of Molecular Medicine, University of Essen, Essen, Germany 3. Physiologisches Institut, der Universit?t Tübingen, Gmelinstr. 5, 72076, Tübingen, Germany
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Abstract: | Bismuth is used for multiple industrial purposes and in the treatment of several gastrointestinal diseases. Untoward effects
of bismuth include anemia, which could, in theory, result from suicidal erythrocyte death or eryptosis. Hallmarks of eryptosis
are cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing
cells are rapidly cleared from circulating blood. Signaling leading to eryptosis includes increase in cytosolic Ca2+ activity and formation of ceramide. The present experiments explored whether bismuth elicits eryptosis. To this end, phosphatidylserine
exposure was estimated from annexin V-binding, cell shrinkage from decrease of forward scatter in FACS analysis, cytosolic
Ca2+ activity from Fluo3 fluorescence and ceramide abundance from binding of fluorescent antibodies. A 48 h exposure to bismuth
(≥500 μg/l BiCl3) enhanced the percentage of annexin V-binding cells and decreased forward scatter, increased cytosolic Ca2+ activity, and stimulated ceramide formation. In conclusion, bismuth stimulates eryptosis, the suicidal death of erythrocytes.
The effect may contribute to or even account for the development of anemia during bismuth treatment. Moreover, ceramide formation
in intestinal cells may participate in the therapeutic efficacy of bismuth preparations.
This study was supported by the Deutsche Forschungsgemeinschaft SFB 766 and the Carl Zeiss Stiftung. The experimental work
and studies on human subjects have been approved by the Ethical commission of the University of Tübingen. |
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Keywords: | Cell volume Annexin Eryptosis Calcium Phosphatidylserine |
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