A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation

Yung Kuo Lin, Yao Chang Chen, Yu Hsun Kao, Chin Feng Tsai, Yung Hsin Yeh, Jin Long Huang, Chen Chuan Cheng, Shih Ann Chen, Yi Jen Chen

Research output: Contribution to journalArticle

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Abstract

Background Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes. Methods Whole-cell patch clamp, indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5 mM) for 24 h. Results Compared to control myocytes (n = 14), OLA-treated myocytes (n = 16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p <0.05) and APD 50 (24 ± 6 vs. 38 ± 4 ms, p <0.05) with a higher incidence of delayed afterdepolarizations (35.7% vs. 7%, p <0.05), which were suppressed by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n = 19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p <0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p <0.05) than control myocytes (n = 15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca2 +-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes. Conclusions MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.

Original languageEnglish
Pages (from-to)191-198
Number of pages8
JournalInternational Journal of Cardiology
Volume176
Issue number1
DOIs
Publication statusPublished - 2014

Fingerprint

Monounsaturated Fatty Acids
Oleic Acid
Muscle Cells
Sodium
Calcium
Sodium-Potassium-Exchanging ATPase
pamidronate
Sodium-Calcium Exchanger
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Calcium Chloride
Calcium-Calmodulin-Dependent Protein Kinases
Calcium-Transporting ATPases
Atrial Fibrillation
Action Potentials
Proteins
Obesity
Fluorescence
Western Blotting
Acids

Keywords

  • Atrial fibrillation
  • Obesity
  • Oleic acid

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation. / Lin, Yung Kuo; Chen, Yao Chang; Kao, Yu Hsun; Tsai, Chin Feng; Yeh, Yung Hsin; Huang, Jin Long; Cheng, Chen Chuan; Chen, Shih Ann; Chen, Yi Jen.

In: International Journal of Cardiology, Vol. 176, No. 1, 2014, p. 191-198.

Research output: Contribution to journalArticle

Lin, Yung Kuo ; Chen, Yao Chang ; Kao, Yu Hsun ; Tsai, Chin Feng ; Yeh, Yung Hsin ; Huang, Jin Long ; Cheng, Chen Chuan ; Chen, Shih Ann ; Chen, Yi Jen. / A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation. In: International Journal of Cardiology. 2014 ; Vol. 176, No. 1. pp. 191-198.
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abstract = "Background Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes. Methods Whole-cell patch clamp, indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5 mM) for 24 h. Results Compared to control myocytes (n = 14), OLA-treated myocytes (n = 16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p <0.05) and APD 50 (24 ± 6 vs. 38 ± 4 ms, p <0.05) with a higher incidence of delayed afterdepolarizations (35.7{\%} vs. 7{\%}, p <0.05), which were suppressed by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n = 19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p <0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p <0.05) than control myocytes (n = 15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca2 +-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes. Conclusions MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.",
keywords = "Atrial fibrillation, Obesity, Oleic acid",
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T1 - A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation

AU - Lin, Yung Kuo

AU - Chen, Yao Chang

AU - Kao, Yu Hsun

AU - Tsai, Chin Feng

AU - Yeh, Yung Hsin

AU - Huang, Jin Long

AU - Cheng, Chen Chuan

AU - Chen, Shih Ann

AU - Chen, Yi Jen

PY - 2014

Y1 - 2014

N2 - Background Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes. Methods Whole-cell patch clamp, indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5 mM) for 24 h. Results Compared to control myocytes (n = 14), OLA-treated myocytes (n = 16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p <0.05) and APD 50 (24 ± 6 vs. 38 ± 4 ms, p <0.05) with a higher incidence of delayed afterdepolarizations (35.7% vs. 7%, p <0.05), which were suppressed by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n = 19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p <0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p <0.05) than control myocytes (n = 15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca2 +-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes. Conclusions MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.

AB - Background Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes. Methods Whole-cell patch clamp, indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5 mM) for 24 h. Results Compared to control myocytes (n = 14), OLA-treated myocytes (n = 16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p <0.05) and APD 50 (24 ± 6 vs. 38 ± 4 ms, p <0.05) with a higher incidence of delayed afterdepolarizations (35.7% vs. 7%, p <0.05), which were suppressed by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n = 19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p <0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p <0.05) than control myocytes (n = 15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca2 +-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes. Conclusions MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.

KW - Atrial fibrillation

KW - Obesity

KW - Oleic acid

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