Browsing by Subject "Sarcoplasmic reticulum"

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    Cellular death linked to irreversible stress in the sarcoplasmic reticulum: the effect of inhibiting Ca(2+) -ATPase or protein glycosylation in the myocardiac cell model H9c2
    (2007-10) Lax Pérez, Antonio Manuel; Fernandez Belda, Francisco; Soler Pardo, Fernando; Medicina
    Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release. The release of cytochrome c was not related with mitochondria depolarization or caspase activation. Irreversible stress in the sarcoplasmic reticulum, detected by the early activation of caspase 12, was functionally linked to the mitochondrial apoptotic pathway. Caspase 3 processing was blocked by cells preincubation with a selective inhibitor of either caspase 9 or caspase 8 whereas caspase 8 activation was inhibited by a selective caspase 9 inhibitor. This was consistent with the involvement of caspase 8 in a positive feedback loop leading to amplify the caspase cascade. Caspase inhibition did not protect against cell death indicating the existence of alternative caspase-independent mechanisms.
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    Passive Ca(2+) overload in H9c2 cardiac myoblasts: assessment of cellular damage and cytosolic Ca(2+) transients
    (Elsevier, 2011-08-15) Lax Pérez, Antonio Manuel; Asensio López, María del Carmen; Pascual Figal, Domingo Andrés; Fernandez Belda, Francisco; Soler Pardo, Fernando; Medicina
    Increase of resting Ca(2+) levels and amplitude of vasopressin-induced Ca(2+) transients were observed when cells in serum-free medium were exposed to 5mM Ca(2+) for 2h. Small effect on cell viability was also observed. A rapid cytotoxic effect was developed in the presence of 10mM Ca(2+) and absence of serum. However, cells exposed to 10mM Ca(2+) in the presence of serum were protected from damage for at least 2days. Resting Ca(2+) levels and cytosolic Ca(2+) transients in serum-containing medium with 10mM Ca(2+) displayed lower increases and a tendency to recover control values. When serum was absent, cells preincubated with 10mM Ca(2+) were more sensitive to thapsigargin-induced damage than cells preincubated with lower Ca(2+). The sensitivity was similar when serum was present. Tolerance to high Ca(2+) in the presence of serum was linked to potentiation of the mitochondrial Ca(2+) entry to decrease the sarcoplasmic reticulum Ca(2+) overload.