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Regulatory volume decrease in cardiomyocytes is modulated by calcium influx and reactive oxygen species
Author(s) -
Rojas-Rivera Diego,
Díaz-Elizondo Jessica,
Parra Valentina,
Salas Daniela,
Contreras Ariel,
Toro Barbra,
Chiong Mario,
Olea-Azar Claudio,
Lavandero Sergio
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.10.003
Subject(s) - reactive oxygen species , nifedipine , catalase , intracellular , chemistry , calcium , myocyte , necrosis , microbiology and biotechnology , medicine , oxidative stress , endocrinology , biochemistry , biology , organic chemistry
We investigated the role of Ca 2+ 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 Ca 2+ . Nifedipine (Nife) inhibited both Hypo‐induced Ca 2+ 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 Ca 2+ influx in the control of cardiomyocyte viability. Hypo‐induced an intracellular Ca 2+ 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.

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