Triggering of Suicidal Erythrocyte Death by CelecoxibReport as inadecuate

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Department of Physiology, University of Tuebingen, Gmelinstraße 5, Tuebingen 72076, Germany


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Abstract The selective cyclooxygenase-2 COX-2 inhibitor celecoxib triggers apoptosis of tumor cells and is thus effective against malignancy. The substance is at least partially effective through mitochondrial depolarization. Even though lacking mitochondria, erythrocytes may enter apoptosis-like suicidal death or eryptosis, which is characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca2+-activity Ca2+i. The present study explored whether celecoxib stimulates eryptosis. Forward scatter was determined to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to depict hemolysis, and Fluo3-fluorescence to quantify Ca2+i. A 48 h exposure of human erythrocytes to celecoxib was followed by significant increase of Ca2+i 15 µM, significant decrease of forward scatter 15 µM and significant increase of annexin-V-binding 10 µM. Celecoxib 15 µM induced annexin-V-binding was blunted but not abrogated by removal of extracellular Ca2+. In conclusion, celecoxib stimulates suicidal erythrocyte death or eryptosis, an effect partially due to stimulation of Ca2+ entry. View Full-Text

Keywords: cell membrane scrambling; phosphatidylserine; calcium; cell volume; eryptosis cell membrane scrambling; phosphatidylserine; calcium; cell volume; eryptosis

Author: Adrian Lupescu, Rosi Bissinger, Kashif Jilani and Florian Lang *



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