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Cardiotrophin-1 induces sarcoplasmic reticulum Ca 2+ leak and arrhythmogenesis in adult rat ventricular myocytes

AuthorsRuiz-Hurtado, Gema; Calderón-Sánchez, Eva; Smani, Tarik; Ordóñez Fernández, Antonio ; Boscá, Lisardo ; Delgado, Carmen
Issue Date2012
PublisherOxford University Press
CitationCardiovascular Research 96(1): 81-89 (2012)
Abstract[Aims]: 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 (ICaL) 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 2060 min induced a significant increase in ICaL density, [Ca 2+]i transients, and cell shortening compared with control cells. Our study reveals that CT-1 increases ICaL 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. © 2012 The Author.
Descriptionet al.
Identifiersdoi: 10.1093/cvr/cvs234
issn: 0008-6363
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