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

Autor: Liu CH; Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung, 804201, Taiwan; Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, 80284, Taiwan., Wen ZH; Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung, 804201, Taiwan; Institute of BioPharmaceutical Sciences, National Sun Yat-Sen University, Kaohsiung, 804201, Taiwan., Huo YN; Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan., Lin CY; Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan., Yang HY; Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan. Electronic address: alfie0314@mail.ndmctsgh.edu.tw., Tsai CS; Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department and Graduate Institute of Pharmacology, National Defense Medical Center, Taipei, Taiwan.
Jazyk: angličtina
Zdroj: European journal of pharmacology [Eur J Pharmacol] 2024 Aug 05; Vol. 976, pp. 176695. Date of Electronic Publication: 2024 May 29.
DOI: 10.1016/j.ejphar.2024.176695
Abstrakt: Lipopolysaccharide (LPS) triggers an inflammatory response, causing impairment of cardiomyocyte Ca 2+ and Na  +  regulation. This study aimed to determine whether piscidin-1 (PCD-1), an antimicrobial peptide, improves intracellular Ca 2+ and Na  +  regulation in LPS-challenged atrial cardiomyocytes. Rabbit atrial cardiomyocytes were enzymatically isolated from the left atria. Patch-clamp ionic current recording, intracellular Ca 2+ 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 Ca 2+ channel currents and larger Na + /Ca 2+ 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 Ca 2+ transient amplitudes and decreased Ca 2+ stores and greater Ca 2+ leakage in the sarcoplasmic reticulum compared to the control. Exposure to PCD-1 attenuated LPS-induced alterations in Ca 2+ 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 Ca 2+ ATPase 2a protein levels were observed in LPS-challenged cardiomyocytes. PCD-1 modulates LPS-induced alterations in inflammatory and Ca 2+ regulatory protein levels. Our results suggest that PCD-1 modulates LPS-induced alterations in intracellular Ca 2+ and Na  +  homeostasis, reactive oxygen species production, and the NF-κB inflammatory pathway in atrial cardiomyocytes.
Competing Interests: 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.
(Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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