Depolarization of Endothelial Cells Enhances Platelet Aggregation Through Oxidative Inactivation of Endothelial NTPDase
| Autor: | Ulrich Pohl, Hae Young Sohn, Torsten Gloe, Steffen-Sebastian Bolz, Matthias Keller, Florian Krötz, Bernhard F. Becker |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Umbilical Veins
Platelet Aggregation Endothelium Cell Survival Blotting Western Umbilical vein Cell Line Membrane Potentials Phosphates Superoxide dismutase chemistry.chemical_compound Antigens CD Superoxides Cricetinae medicine Animals Humans Ectonucleotidase Platelet Mesocricetus biology Chemistry Superoxide Apyrase Depolarization Molecular biology Adenosine Diphosphate Endothelial stem cell Arterioles medicine.anatomical_structure Biochemistry Culture Media Conditioned biology.protein Endothelium Vascular Enzyme Repression Cardiology and Cardiovascular Medicine Oxidation-Reduction |
| Zdroj: | Arteriosclerosis, Thrombosis, and Vascular Biology. 22:2003-2009 |
| ISSN: | 1524-4636 1079-5642 |
| DOI: | 10.1161/01.atv.0000043454.08172.51 |
| Popis: | Objective— The objective of this study was to investigate whether depolarization of cultured endothelial cells (human umbilical vein endothelial cells, HUVECs) affects their ectonucleotidase activity through superoxide (O 2 − ) production. Methods and Results— Depolarization by the cation channel gramicidin (100 nmol/L) or tetrabutylammonium chloride (1 mmol/L) induced O 2 − release from HUVECs (n=4), which was decreased by superoxide dismutase (SOD, 500 U/mL). The activity of endothelial ectonucleotidases was assessed by the production of inorganic phosphate from ADP, which was decreased by chronic depolarization by 25% (n=6, P P Conclusions— Depolarization causes the endothelial production of O 2 − , which inhibits the activity of endothelial ectonucleotidases. Increases in transmural pressure induce endothelial depolarization. In chronically hypertensive diseases, depolarization might favor platelet aggregation. |
| Databáze: | OpenAIRE |
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