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Authordc.contributor.authorRojas Rivera, Andrés 
Authordc.contributor.authorDíaz Elizondo, Jessica es_CL
Authordc.contributor.authorParra Ortíz, María Valentina es_CL
Authordc.contributor.authorSalas, Daniela es_CL
Authordc.contributor.authorContreras Ferrat, Ariel Eduardo es_CL
Authordc.contributor.authorToro, Barbra es_CL
Authordc.contributor.authorChiong Lay, Mario es_CL
Authordc.contributor.authorOlea Azar, Claudio es_CL
Authordc.contributor.authorLavandero González, Sergio es_CL
Admission datedc.date.accessioned2010-06-09T20:32:36Z
Available datedc.date.available2010-06-09T20:32:36Z
Publication datedc.date.issued2009-11-03
Cita de ítemdc.identifier.citationFEBS LETTERS 583 (21): 3485-3492en_US
Identifierdc.identifier.issn0014-5793
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/120984
Abstractdc.description.abstractWe 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.en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherELSEVIER SCIENCE BVen_US
Keywordsdc.subjectCa2+en_US
Títulodc.titleRegulatory volume decrease in cardiomyocytes is modulated by calcium influx and reactive oxygen speciesen_US
Document typedc.typeArtículo de revistaen_US


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