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