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. 2024 Aug 5:976:176695.
doi: 10.1016/j.ejphar.2024.176695. Epub 2024 May 29.

Piscidin-1 regulates lipopolysaccharide-induced intracellular calcium, sodium dysregulation, and oxidative stress in atrial cardiomyocytes

Ching-Han Liu  1 , Zhi-Hong Wen  2 , Yen-Nien Huo  3 , Chih-Yuan Lin  4 , Hsiang-Yu Yang  5 , Chien-Sung Tsai  6
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Free article

Piscidin-1 regulates lipopolysaccharide-induced intracellular calcium, sodium dysregulation, and oxidative stress in atrial cardiomyocytes

Ching-Han Liu et al. Eur J Pharmacol. .
Free article

Abstract

Lipopolysaccharide (LPS) triggers an inflammatory response, causing impairment of cardiomyocyte Ca2+ and Na + regulation. This study aimed to determine whether piscidin-1 (PCD-1), an antimicrobial peptide, improves intracellular Ca2+ and Na + regulation in LPS-challenged atrial cardiomyocytes. Rabbit atrial cardiomyocytes were enzymatically isolated from the left atria. Patch-clamp ionic current recording, intracellular Ca2+ monitoring using Fluo-3, and detection of cytosolic reactive oxygen species production were conducted in control, LPS-challenged, and LPS + PCD-1-treated atrial cardiomyocytes. LPS-challenged cardiomyocytes showed shortened durations of action potential at their 50% and 90% repolarizations, which was reversed by PCD-1 treatment. LPS-challenged cardiomyocytes showed decreased L-type Ca2+ channel currents and larger Na+/Ca2+ exchange currents compared to controls. While LPS did not affect the sodium current, an enhanced late sodium current with increased cytosolic Na+ levels was observed in LPS-challenged cardiomyocytes. These LPS-induced alterations in the ionic current were ameliorated by PCD-1 treatment. LPS-challenged cardiomyocytes displayed lowered Ca2+ transient amplitudes and decreased Ca2+ stores and greater Ca2+ leakage in the sarcoplasmic reticulum compared to the control. Exposure to PCD-1 attenuated LPS-induced alterations in Ca2+ regulation. The elevated reactive oxygen species levels observed in LPS-challenged myocytes were suppressed after PCD-1 treatment. The protein levels of NF-κB and IL-6 increased following LPS treatment. Decreased sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a protein levels were observed in LPS-challenged cardiomyocytes. PCD-1 modulates LPS-induced alterations in inflammatory and Ca2+ regulatory protein levels. Our results suggest that PCD-1 modulates LPS-induced alterations in intracellular Ca2+ and Na + homeostasis, reactive oxygen species production, and the NF-κB inflammatory pathway in atrial cardiomyocytes.

Keywords: Atrial fibrillation; Calcium and sodium regulation; Lipopolysaccharide; Piscidin-1.

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Conflict of interest statement

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Chih-Yuan Lin reports article publishing charges, equipment, drugs, or supplies, statistical analysis, and writing assistance were provided by Ministry of Science and Technology of Taiwan. Hsiang-Yu Yang reports article publishing charges, equipment, drugs, or supplies, statistical analysis, and writing assistance were provided by Ministry of National Defense Medical Affairs Bureau. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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