Involvement of ceramide in hyperosmotic shock-induced death of erythrocytes.

Lang, K S, Mysina, Svetlana, Brand, V, Sandu, C, Lang, P A, Berchtold, S, Huber, S M, Lang, F and Wieder, T (2004) Involvement of ceramide in hyperosmotic shock-induced death of erythrocytes. Cell death and differentiation, 11 (2). pp. 231-43. ISSN 1350-9047

Full text not available from this repository. (Request a copy)

Abstract

Erythrocytes lack nuclei and mitochondria, the organelles important for apoptosis of nucleated cells. However, following increase of cytosolic Ca(2+) activity, erythrocytes undergo cell shrinkage, cell membrane blebbing and breakdown of phosphatidylserine asymmetry, all features typical for apoptosis in nucleated cells. The same events are observed following osmotic shock, an effect mediated in part by activation of Ca(2+)-permeable cation channels. However, erythrocyte death following osmotic shock is blunted but not prevented in the absence of extracellular Ca(2+) pointing to additional mechanisms. As shown in this study, osmotic shock (950 mOsm) triggers sphingomyelin breakdown and formation of ceramide. The stimulation of annexin binding following osmotic shock is mimicked by addition of ceramide or purified sphingomyelinase and significantly blunted by genetic (aSM-deficient mice) or pharmacologic (50 microM 3,4-dichloroisocoumarin) knockout of sphingomyelinase. The effect of ceramide is blunted but not abolished in the absence of Ca(2+). Conversely, osmotic shock-induced annexin binding is potentiated in the presence of sublethal concentrations of ceramide. In conclusion, ceramide and Ca(2+) entry through cation channels concert to trigger erythrocyte death during osmotic shock.

Item Type: Article
Subjects: Sciences > Biomedical Sciences
Depositing User: Svetlana Mysina
Date Deposited: 08 Oct 2018 09:10
Last Modified: 09 Oct 2018 10:29
URI: http://sure.sunderland.ac.uk/id/eprint/10028

Actions (login required)

View Item View Item