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Cation channels, cell volume and the death of an erythrocyte.

Lang, Florian, Lang, Karl S, Wieder, Thomas, Mysina, Svetlana, Birka, Christina, Lang, Philipp A, Kaiser, Stephanie, Kempe, Daniela, Duranton, Christophe and Huber, Stephan M (2003) Cation channels, cell volume and the death of an erythrocyte. Pflugers Archiv : European journal of physiology, 447 (2). pp. 121-5. ISSN 0031-6768

Item Type: Article

Abstract

Similar to a variety of nucleated cells, human erythrocytes activate a non-selective cation channel upon osmotic cell shrinkage. Further stimuli of channel activation include oxidative stress, energy depletion and extracellular removal of Cl-. The channel is permeable to Ca2+ and opening of the channel increases cytosolic [Ca2+]. Intriguing evidence points to a role of this channel in the elimination of erythrocytes by apoptosis. Ca2+ entering through the cation channel stimulates a scramblase, leading to breakdown of cell membrane phosphatidylserine asymmetry, and stimulates Ca(2+)-sensitive K+ channels, thus leading to KCl loss and (further) cell shrinkage. The breakdown of phosphatidylserine asymmetry is evidenced by annexin binding, a typical feature of apoptotic cells. The effects of osmotic shock, oxidative stress and energy depletion on annexin binding are mimicked by the Ca2+ ionophore ionomycin (1 microM) and blunted in the nominal absence of extracellular Ca2+. Nevertheless, the residual annexin binding points to additional mechanisms involved in the triggering of the scramblase. The exposure of phosphatidylserine at the extracellular face of the cell membrane stimulates phagocytes to engulf the apoptotic erythrocytes. Thus, sustained activation of the cation channels eventually leads to clearance of affected erythrocytes from peripheral blood. Susceptibility to annexin binding is enhanced in several genetic disorders affecting erythrocyte function, such as thalassaemia, sickle-cell disease and glucose-6-phosphate dehydrogenase deficiency. The enhanced vulnerability presumably contributes to the shortened life span of the affected erythrocytes. Beyond their role in the limitation of erythrocyte survival, cation channels may contribute to the triggering of apoptosis in nucleated cells exposed to osmotic shock and/or oxidative stress.

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More Information

Depositing User: Svetlana Mysina

Identifiers

Item ID: 10029
ISSN: 0031-6768
URI: http://sure.sunderland.ac.uk/id/eprint/10029

Users with ORCIDS

Catalogue record

Date Deposited: 08 Oct 2018 09:05
Last Modified: 09 Oct 2018 11:03

Contributors

Author: Florian Lang
Author: Karl S Lang
Author: Thomas Wieder
Author: Svetlana Mysina
Author: Christina Birka
Author: Philipp A Lang
Author: Stephanie Kaiser
Author: Daniela Kempe
Author: Christophe Duranton
Author: Stephan M Huber

Subjects

Sciences > Biomedical Sciences

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