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Cation channels trigger apoptotic death of erythrocytes.

Lang, K S, Duranton, C, Poehlmann, H, Mysina, Svetlana, Bauer, C, Lang, F, Wieder, T and Huber, S M (2003) Cation channels trigger apoptotic death of erythrocytes. Cell death and differentiation, 10 (2). pp. 249-56. ISSN 1350-9047

Item Type: Article

Abstract

Erythrocytes are devoid of mitochondria and nuclei and were considered unable to undergo apoptosis. As shown recently, however, the Ca(2+)-ionophore ionomycin triggers breakdown of phosphatidylserine asymmetry (leading to annexin binding), membrane blebbing and shrinkage of erythrocytes, features typical for apoptosis in nucleated cells. In the present study, the effects of osmotic shrinkage and oxidative stress, well-known triggers of apoptosis in nucleated cells, were studied. Exposure to 850 mOsm for 24 h, to tert-butyl-hydroperoxide (1 mM) for 15 min, or to glucose-free medium for 48 h, all elicit erythrocyte shrinkage and annexin binding, both sequelae being blunted by removal of extracellular Ca(2+) and mimicked by ionomycin (1 microM). Osmotic shrinkage and oxidative stress activate Ca(2+)-permeable cation channels and increase cytosolic Ca(2+) concentration. The channels are inhibited by amiloride (1 mM), which further blunts annexin binding following osmotic shock, oxidative stress and glucose depletion. In conclusion, osmotic and oxidative stress open Ca(2+)-permeable cation channels in erythrocytes, thus increasing cytosolic Ca(2+) activity and triggering erythrocyte apoptosis.

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More Information

Depositing User: Svetlana Mysina

Identifiers

Item ID: 10030
ISSN: 1350-9047
URI: http://sure.sunderland.ac.uk/id/eprint/10030

Users with ORCIDS

ORCID for Svetlana Mysina: ORCID iD orcid.org/0000-0003-3818-3255

Catalogue record

Date Deposited: 08 Oct 2018 09:04
Last Modified: 09 Oct 2018 10:29

Contributors

Author: Svetlana Mysina ORCID iD
Author: K S Lang
Author: C Duranton
Author: H Poehlmann
Author: C Bauer
Author: F Lang
Author: T Wieder
Author: S M Huber

Subjects

Sciences > Biomedical Sciences

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