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First published online 1 March 2005
doi: 10.1242/jcs.01730
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Research Article |
1 Department of Physiology, University of Tübingen, Germany
2 Department of Radiation Oncology, University of Tübingen, Germany
3 Department of Biochemistry and Molecular Biology, University of Tokyo, Japan
4 Department of Anesthesiology and Transfusion Medicine, University of Tübingen, Germany
* Author for correspondence (e-mail: florian.lang{at}uni-tuebingen.de)
Accepted 14 January 2005
Osmotic erythrocyte shrinkage leads to activation of cation channels with subsequent Ca2+ entry and stimulates a sphingomyelinase with subsequent formation of ceramide. Ca2+ and ceramide then activate a scramblase leading to breakdown of phosphatidylserine asymmetry of the cell membrane. The mediators accounting for activation of erythrocyte sphingomyelinase and phosphatidylserine exposure remained elusive. The study demonstrates that platelet-activating factor (PAF) is released from erythrocytes upon hyperosmotic cell shrinkage. The experiments further disclose the presence of PAF receptors in erythrocytes and show that PAF stimulates the breakdown of sphingomyelin and the release of ceramide from erythrocytes at isotonic conditions. PAF further triggers cell shrinkage (decrease of forward scatter) and phosphatidylserine exposure (annexin binding) of erythrocytes. The stimulation of annexin-binding is blunted by a genetic knockout of PAF receptors, by the PAF receptor antagonist ABT491 or by inhibition of sphingomyelinase with urea. In conclusion, PAF activates an erythrocyte sphingomyelinase and the then formed ceramide leads to the activation of scramblase with subsequent phosphatidylserine exposure.
Key words: Cell volume, Annexin, Apoptosis, Sphingomyelinase, Phosphatidylserine
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