Regulatory volume decrease in cardiomyocytes is modulated by calcium influx and reactive oxygen species
| Autor: | Diego Rojas-Rivera, Mario Chiong, Barbra Toro, Daniela Salas, Claudio Olea-Azar, Jessica Díaz-Elizondo, Sergio Lavandero, Valentina Parra, Ariel Contreras |
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| Rok vydání: | 2009 |
| Předmět: |
Osmotic stress
Cytoplasm Ruthenium red Necrosis Cell Survival Biophysics Cardiomyocyte Biochemistry Gene Expression Regulation Enzymologic Rats Sprague-Dawley chemistry.chemical_compound Osmotic Pressure Structural Biology Genetics medicine Animals Myocytes Cardiac Molecular Biology Cells Cultured Cell Size chemistry.chemical_classification Reactive oxygen species biology Superoxide Volume regulation nutritional and metabolic diseases Biological Transport ROS Heart Cell Biology Catalase Rats Cell biology Ca2+ chemistry Ionomycin biology.protein Calcium medicine.symptom Reactive Oxygen Species Intracellular Peroxynitrite |
| Zdroj: | FEBS Letters. 583:3485-3492 |
| ISSN: | 0014-5793 |
| Popis: | We investigated the role of Ca2+ in generating reactive oxygen species (ROS) induced by hyposmotic stress (Hypo) and its relationship to regulatory volume decrease (RVD) in cardiomyocytes. Hypo-induced increases in cytoplasmic and mitochondrial Ca2+. Nifedipine (Nife) inhibited both Hypo-induced Ca2+ and ROS increases. Overexpression of catalase (CAT) induced RVD and a decrease in Hypo-induced blebs. Nife prevented CAT-dependent RVD activation. These results show a dual role of Hypo-induced Ca2+ influx in the control of cardiomyocyte viability. Hypo-induced an intracellular Ca2+ increase which activated RVD and inhibited necrotic blebbing thus favoring cell survival, while simultaneously increasing ROS generation, which in turn inhibited RVD and induced necrosis. |
| Databáze: | OpenAIRE |
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