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Cardiac Cell Hypertrophy In Vitro
Author(s) -
Colella Matilde,
Pozzan Tullio
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1420.008
Subject(s) - nfat , medicine , endocrinology , calcineurin , muscle hypertrophy , receptor , chemistry , in vitro , angiotensin ii , microbiology and biotechnology , biophysics , biology , biochemistry , transplantation
Various conditions were used to investigate the importance of Ca 2+ signaling in triggering hypertrophy in neonatal rat cardiomyocytes in vitro . An increase in cell size and sarcomere reorganization were induced not only by treatment with receptor agonists, such as angiotensin II, aldosterone, and norepinephrine, but also by a small depolarization caused by an increase in the KCl concentration of the medium. This latter treatment has no direct effects on receptor signaling. All these hypertrophic treatments caused a long‐lasting increase in the frequency of spontaneous [Ca 2+ ] oscillations, causing nuclear translocation of transfected NFAT (GFP). Cyclosporine A inhibited hypertrophy and NFAT translocation, but not the increased oscillation frequency. We propose here that calcineurin–NFAT can act as integrators of the Ca 2+ signal and can decode alterations in the frequency even of very rapid Ca 2+ oscillations.