Amyloid peptide regulates calcium homoeostasis and arrhythmogenesis in pulmonary vein cardiomyocytes

Hsuan Ming Tsao, Punate Weerateerangkul, Yao Chang Chen, Yu Hsun Kao, Yung Kuo Lin, Jen Hung Huang, Shih Ann Chen, Yi Jen Chen

Research output: Contribution to journalArticle

6 Citations (Scopus)

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 4-6h, using Western blot analysis, indo-1 fluorimetric ratio and whole-cell patch clamp techniques. Aβ 25-35 decreased the expressions of Ca V1.2, 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±5ms, P25-35 has direct electrophysiological effects on PV cardiomyocytes.

Original languageEnglish
Pages (from-to)589-598
Number of pages10
JournalEuropean Journal of Clinical Investigation
Volume42
Issue number6
DOIs
Publication statusPublished - Jun 2012

Fingerprint

Pulmonary Veins
Amyloid
Cardiac Myocytes
Homeostasis
Calcium
Peptides
Sodium-Calcium Exchanger
Sarcoplasmic Reticulum
Atrial Fibrillation
Ryanodine Receptor Calcium Release Channel
Clamping devices
Electric current control
Patch-Clamp Techniques
Calcium Channels
Action Potentials
Adenosine Triphosphatases
Proteins
Western Blotting
Rabbits

Keywords

  • β-amyloid
  • Atrial fibrillation
  • Cardiac amyloidosis
  • Isolated cardiomyocytes
  • Pulmonary vein

ASJC Scopus subject areas

  • Medicine(all)
  • Clinical Biochemistry
  • Biochemistry

Cite this

Amyloid peptide regulates calcium homoeostasis and arrhythmogenesis in pulmonary vein cardiomyocytes. / Tsao, Hsuan Ming; Weerateerangkul, Punate; Chen, Yao Chang; Kao, Yu Hsun; Lin, Yung Kuo; Huang, Jen Hung; Chen, Shih Ann; Chen, Yi Jen.

In: European Journal of Clinical Investigation, Vol. 42, No. 6, 06.2012, p. 589-598.

Research output: Contribution to journalArticle

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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 4-6h, using Western blot analysis, indo-1 fluorimetric ratio and whole-cell patch clamp techniques. Aβ 25-35 decreased the expressions of Ca V1.2, 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±5ms, P25-35 has direct electrophysiological effects on PV cardiomyocytes.",
keywords = "β-amyloid, Atrial fibrillation, Cardiac amyloidosis, Isolated cardiomyocytes, Pulmonary vein",
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AU - Weerateerangkul, Punate

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AU - Lin, Yung Kuo

AU - Huang, Jen Hung

AU - Chen, Shih Ann

AU - Chen, Yi Jen

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N2 - 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 4-6h, using Western blot analysis, indo-1 fluorimetric ratio and whole-cell patch clamp techniques. Aβ 25-35 decreased the expressions of Ca V1.2, 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±5ms, P25-35 has direct electrophysiological effects on PV cardiomyocytes.

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