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Melanocyte‐like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers
Author(s) -
Patel Vickas V,
Levin Mark D,
Lu Min M,
Petrenko Nataliya B,
Gupta Tara H,
Hawkins Brian J,
Buckley Peter T,
Yuan Lijun,
Beermann Friedrich,
Marguiles Kenneth B,
Muniswamy Madesh,
Eberwine James H,
Epstein Jonathan A
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.180.4
Subject(s) - cardiac arrhythmia , melanocyte , medicine , afterdepolarization , atrium (architecture) , atrial fibrillation , cardiology , biology , electrophysiology , repolarization , cancer research , melanoma
Atrial fibrillation is the most common clinical cardiac arrhythmia. It is often initiated by ectopic beats arising from the pulmonary veins and atrium, but the source of these beats remains unclear. Here, we report detailed analysis of a cell population within murine and human hearts that displays spatial and cellular characteristics suggesting they contribute to atrial arrhythmia triggers. These cells express genes of the melanocyte lineage, including dopachrome tautomerase (Dct), and populate the pulmonary veins, atria and atrioventricular canal in murine hearts. Murine cardiac melanocyte‐like cells express adrenergic and muscarinic receptors and display transcriptional profiles distinct from dermal melanocytes. Adult mice lacking the gene encoding Dct display increased susceptibility to atrial arrhythmias, despite having structurally normal hearts. Kit mutant mice lacking cardiac melanocyte‐like cells do not develop atrial arrhythmias in the absence of Dct, suggesting that a derangement within these cells, and not their absence promotes arrhythmias. Cardiac melanocyte‐like cells are excitable and those lacking Dct have prolonged repolarization with early afterdepolarizations. Dct‐expressing cells are present in human hearts where atrial arrhythmias can arise. Thus, we propose melanocyte‐like cells in the atrium and pulmonary veins may contribute to atrial arrhythmias in some patients.