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Amyloid peptide regulates calcium homoeostasis and arrhythmogenesis in pulmonary vein cardiomyocytes
Author(s) -
Tsao HsuanMing,
Weerateerangkul Punate,
Chen YaoChang,
Kao YuHsun,
Lin YungKuo,
Huang JenHung,
Chen ShihAnn,
Chen YiJen
Publication year - 2012
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2011.02618.x
Subject(s) - phospholamban , ryanodine receptor , calcium , medicine , calcium atpase , homeostasis , chemistry , endocrinology , calcium in biology , calcium metabolism , sodium calcium exchanger , patch clamp , atrial fibrillation , electrophysiology , biology , biochemistry , atpase , enzyme
Eur J Clin Invest 2012; 42 (6): 589–598 Abstract 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 (Aβ 25–35 ) for 4–6 h, using Western blot analysis, indo‐1 fluorimetric ratio and whole‐cell patch clamp techniques. Aβ 25–35 decreased the expressions of Ca V 1.2, 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). Aβ 25–35 ‐treated cardiomyocytes had smaller calcium transient, SR calcium store, L‐type calcium current and sodium/calcium exchanger current than control cardiomyocytes. Moreover, Aβ 25–35 ‐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 Aβ 25–35 has direct electrophysiological effects on PV cardiomyocytes.