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Prostaglandin E2 activates channel-mediated calcium entry in human erythrocytes: an indication for a blood clot formation supporting process.

作者信息

Kaestner Lars, Tabellion Wiebke, Lipp Peter, Bernhardt Ingolf

机构信息

Institute for Molecular Cell Biology, Faculty of Medicine, Building 61, Saarland University, 66421 Homburg/Saar, Germany.

出版信息

Thromb Haemost. 2004 Dec;92(6):1269-72. doi: 10.1160/TH04-06-0338.

Abstract

Prostaglandin E(2) (PGE(2)) is released from platelets when they are activated. Using fluorescence imaging and the patch-clamp technique, we provide evidence that PGE(2) 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 PGE(2) responses of red blood cells described here reveal a direct and active participation of erythrocytes in blood clot formation.

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