Amyloid peptide regulates calcium homoeostasis and arrhythmogenesis in pulmonary vein cardiomyocytes
Correction(s) for this article
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Corrigendum
- Volume 46Issue 7European Journal of Clinical Investigation
- pages: 676-676
- First Published online: June 26, 2016
Hsuan-Ming Tsao
Division of Cardiology, National Yang-Ming University Hospital, I-Lan, Taiwan
Search for more papers by this authorPunate Weerateerangkul
Department of Physiology, Faculty of Medicine, Cardiac Electrophysiology Research and Training Center, Chiang Mai University, Thailand
Search for more papers by this authorYao-Chang Chen
Department of Biomedical Engineering, National Defense Medical Center
Search for more papers by this authorYung-Kuo Lin
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorJen-Hung Huang
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorShih-Ann Chen
Division of Cardiology and Cardiovascular Research Center, Taipei Veterans General Hospital, Taipei, Taiwan
Search for more papers by this authorYi-Jen Chen
Graduate Institute of Clinical Medicine
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorHsuan-Ming Tsao
Division of Cardiology, National Yang-Ming University Hospital, I-Lan, Taiwan
Search for more papers by this authorPunate Weerateerangkul
Department of Physiology, Faculty of Medicine, Cardiac Electrophysiology Research and Training Center, Chiang Mai University, Thailand
Search for more papers by this authorYao-Chang Chen
Department of Biomedical Engineering, National Defense Medical Center
Search for more papers by this authorYung-Kuo Lin
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorJen-Hung Huang
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorShih-Ann Chen
Division of Cardiology and Cardiovascular Research Center, Taipei Veterans General Hospital, Taipei, Taiwan
Search for more papers by this authorYi-Jen Chen
Graduate Institute of Clinical Medicine
Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University
Search for more papers by this authorAbstract
Eur J Clin Invest 2012; 42 (6): 589–598
Background Amyloid peptides modulate cardiac calcium homoeostasis and play an important role in the pathophysiology of atrial fibrillation. Pulmonary veins (PVs) are critical in the genesis of atrial fibrillation and contain abundant amyloid peptides. Therefore, the purpose of this study is to investigate whether amyloid peptides may change the PV electrical activity through regulating calcium homoeostasis.
Methods and results The channel and calcium-handling protein expressions, intracellular calcium and ionic currents were studied in isolated rabbit PV cardiomyocytes in the presence and absence (control) of beta-amyloid (Aβ25–35) for 4–6 h, using Western blot analysis, indo-1 fluorimetric ratio and whole-cell patch clamp techniques. Aβ25–35 decreased the expressions of CaV1.2, total or Ser16-phosphorylated phospholamban (p-PLB), p-PLB/PLB ratio, sodium/calcium exchanger, but did not change ryanodine receptor, sarcoplasmic reticulum (SR) ATPase and K+ channel proteins (Kir2.1, Kir2.3, Kv1.4, Kv1.5 and Kv4.2). Aβ25–35-treated cardiomyocytes had smaller calcium transient, SR calcium store, L-type calcium current and sodium/calcium exchanger current than control cardiomyocytes. Moreover, Aβ25–35-treated cardiomyocytes (n = 20) had shorter 90% of the action potential duration (82 ± 3 vs. 93 ± 5 ms, P < 0·05) than control cardiomyocytes (n = 16).
Conclusion Aβ25–35 has direct electrophysiological effects on PV cardiomyocytes.
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