Thromb Haemost 2004; 92(06): 1269-1272
DOI: 10.1160/TH04-06-0338
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Prostaglandin E2 activates channel-mediated calcium entry in human erythrocytes: an indication for a blood clot formation supporting process

Lars Kaestner
1   Institute for Molecular Cell Biology, Faculty of Medicine, Saarland University, Homburg/Saar, Germany
,
Wiebke Tabellion
1   Institute for Molecular Cell Biology, Faculty of Medicine, Saarland University, Homburg/Saar, Germany
2   Laboratory of Biophysics, Faculty of Natural and Technical Sciences III, Saarland University, Saarbrücken, Germany
,
Peter Lipp
1   Institute for Molecular Cell Biology, Faculty of Medicine, Saarland University, Homburg/Saar, Germany
,
Ingolf Bernhardt
2   Laboratory of Biophysics, Faculty of Natural and Technical Sciences III, Saarland University, Saarbrücken, Germany
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Publikationsverlauf

Received 02. Juni 2004

Accepted after revision 09. September 2004

Publikationsdatum:
02. Dezember 2017 (online)

Summary

Prostaglandin E2 (PGE2) is released from platelets when they are activated. Using fluorescence imaging and the patch-clamp technique, we provide evidence that PGE2 at physiological concentrations (10−10 M) activates calcium rises mediated by calcium influx through a non-selective cation-channel in human red blood cells. The extent of calcium increase varied between cells with a total of 45% of the cells responding. It is well known that calcium increases elicited the calcium-activated potassium channel (Gardos channel) in the red cell membrane. Previously, it was shown that the Gardos channel activation results in potassium efflux and shrinkage of the cells. Therefore, we conclude that the PGE2 responses of red blood cells described here reveal a direct and active participation of erythrocytes in blood clot formation.

 
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