000 | 02576na a2200229 4500 | ||
---|---|---|---|
003 | PC6679 | ||
005 | 20210625062804.0 | ||
008 | 130622s2012 xxx||||| |||| 00| 0 eng d | ||
040 | _cH12O | ||
041 | _aeng | ||
100 |
_aRuiz Hurtado, Gema _92167 _eInstituto de Investigación i+12 |
||
245 | 0 | 0 |
_aCardiotrophin-1 induces sarcoplasmic reticulum Ca2+ leak and arrhythmogenesis in adult rat ventricular myocytes. _h[artículo] |
260 |
_bCardiovascular Research, _c2012 |
||
300 | _a96(1):81-9. | ||
500 | _aFormato Vancouver: Ruiz-Hurtado G, Gómez-Hurtado N, Fernández-Velasco M, Calderón E, Smani T, Ordoñez A et al. Cardiotrophin-1 induces sarcoplasmic reticulum Ca(2+) leak and arrhythmogenesis in adult rat ventricular myocytes. Cardiovasc Res. 2012 Oct 1;96(1):81-9. | ||
501 | _aPMID: 22787135 | ||
504 | _aContiene 55 referencias | ||
520 | _aAIMS: Plasma levels of cardiotrophin-1 (CT-1) are elevated in several cardiovascular diseases and are correlated with the severity of the pathology. However, the mechanisms by which this inflammatory cytokine participates in the pathology of the heart are not completely understood. It is well established that alterations in intracellular calcium ([Ca(2+)](i)) handling are involved in cardiac dysfunction during heart failure, but it is unknown whether CT-1 modulates [Ca(2+)](i) handling in adult cardiomyocytes. Here we have analyzed for the first time the effects of CT-1 on [Ca(2+)](i) homeostasis in adult rat cardiomyocytes. METHODS AND RESULTS: L-type calcium current (I(CaL)) was recorded using patch-clamp techniques, and [Ca(2+)](i) transients and Ca(2+) sparks were viewed by confocal microscopy. Treatment of cardiomyocytes with 1 nM CT-1 for 20-60 min induced a significant increase in I(CaL) density, [Ca(2+)](i) transients, and cell shortening compared with control cells. Our study reveals that CT-1 increases I(CaL) by a protein kinase A-dependent mechanism, and Ca(2+) sparks by a Ca(2+)/calmodulin kinase II-dependent and protein kinase A-independent mechanism. Cardiomyocytes treated with CT-1 exhibited a higher occurrence of arrhythmogenic behaviour, manifested as spontaneous Ca(2+) waves and aftercontractions. CONCLUSION: Our findings provide evidence that cardiomyocytes treated with CT-1 present high spontaneous Ca(2+) release during diastole, a mechanism linked to arrhythmogenicity in the pathologic heart. | ||
710 |
_9625 _aInstituto de Investigación imas12 |
||
856 |
_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/6/pc6679.pdf _ySolicitar documento |
||
942 |
_n0 _2ddc _cART |
||
999 |
_c6679 _d6679 |