The fully linked HTML version of this article has now been published.
JCS ePress
online publication date 1 Mar 2005
doi: 10.1242/jcs.01730
Research Article
Stimulation of erythrocyte ceramide formation by platelet-activating factor
Philipp A. Lang,
Daniela S. Kempe,
Valerie Tanneur,
Kerstin Eisele,
Barbara A. Klarl,
Svetlana Myssina,
Verena Jendrossek,
Satoshi Ishii,
Takao Shimizu,
Marc Waidmann,
Gabriele Hessler,
Stephan M. Huber,
Florian Lang*,
and
Thomas Wieder
* Author for correspondence (e-mail: florian.lang{at}uni-tuebingen.de)
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.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
|
|
 
S. Uhlig and E. Gulbins
Sphingolipids in the Lungs
Am. J. Respir. Crit. Care Med.,
December 1, 2008;
178(11):
1100 - 1114.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Kiedaisch, A. Akel, O. M Niemoeller, T. Wieder, and F. Lang
Zinc-induced suicidal erythrocyte death
Am. J. Clinical Nutrition,
May 1, 2008;
87(5):
1530 - 1534.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Foller, R. S. Kasinathan, S. Koka, S. M. Huber, B. Schuler, J. Vogel, M. Gassmann, and F. Lang
Enhanced susceptibility to suicidal death of erythrocytes from transgenic mice overexpressing erythropoietin
Am J Physiol Regulatory Integrative Comp Physiol,
September 1, 2007;
293(3):
R1127 - R1134.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Hermle, E. Shumilina, P. Attanasio, A. Akel, D. S. Kempe, P. A. Lang, M. Podolski, S. Gatz, R. Bachmann, C. Bachmann, et al.
Decreased cation channel activity and blunted channel-dependent eryptosis in neonatal erythrocytes
Am J Physiol Cell Physiol,
October 1, 2006;
291(4):
C710 - C717.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Gulbins and P. L. Li
Physiological and pathophysiological aspects of ceramide
Am J Physiol Regulatory Integrative Comp Physiol,
January 1, 2006;
290(1):
R11 - R26.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. A. Klarl, P. A. Lang, D. S. Kempe, O. M. Niemoeller, A. Akel, M. Sobiesiak, K. Eisele, M. Podolski, S. M. Huber, T. Wieder, et al.
Protein kinase C mediates erythrocyte "programmed cell death" following glucose depletion
Am J Physiol Cell Physiol,
January 1, 2006;
290(1):
C244 - C253.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Karasawa, M. Shirakura, A. Harada, N. Satoh, K. Yokoyama, M. Setaka, and K. Inoue
Red Blood Cells Highly Express Type I Platelet-Activating Factor-Acetylhydrolase (PAF-AH) Which Consists of the {alpha}1/{alpha}2 Complex
J. Biochem.,
October 1, 2005;
138(4):
509 - 517.
[Abstract]
[Full Text]
[PDF]
|
|
|
© The Company of Biologists Ltd 2005
