Literature DB >> 22777069

Electrophysiological effects of lysophosphatidylcholine on HL-1 cardiomyocytes assessed with a microelectrode array system.

Sigfus Gizurarson1, Yangzhen Shao, Azra Miljanovic, Truls Råmunddal, Jan Borén, Lennart Bergfeldt, Elmir Omerovic.   

Abstract

BACKGROUND: Sudden death due to malignant ventricular arrhythmias is the most important cause of death in acute myocardial infarction. Improved knowledge about the pathophysiology underlying these arrhythmias is essential in the search for new anti-arrhythmic strategies. Lysophosphatidylcholine (LPC), a hydrolysis product of (membrane) phospholipid degradation, is one of the most potent pro-arrhythmic substances that accumulate in the human heart during myocardial ischemia. The aim of this study was to set up and validate an in vitro experimental system for studies on the effects of LPC on electrophysiological parameters in beating cardiomyocytes. METHODS AND
RESULTS: Spontaneously beating HL-1 cardiomyocytes were cultured on multielectrode array microchips for three days for the recording of electrical activities in the form of field potentials (FP). FPs were recorded at baseline and after addition of 2, 4, 8, 12, 16, 20, and 24 µM of LPC to the cell medium (n=9). We found that LPC could induce rapid effects on electrical parameters in the HL-1 cells. The overall half-maximal effective concentration (EC(50)) of LPC was around 12 µM. The beating rate and peak-peak amplitude of FP thus decreased at concentrations ≥ 12 µM and were inversely proportional to increased LPC concentration. The duration of FP was significantly prolonged with LPC above 12 µM and was concentration-dependent. LPC delayed signal propagation, an effect which was mimicked by blocking gap junctions with heptanol and attenuated by pre-treatment with isoprenaline and atropine. Finally, asynchronous activity was induced by LPC at >12 µM.
CONCLUSIONS: LPC induced prompt and pronounced electrophysiological alterations that may underlie its observed pro-arrhythmic properties. Our in vitro model with HL-1 cells and microelectrode array system may be a useful tool for preclinical studies of electrophysiological effects of various pathophysiological concepts.
Copyright © 2012 S. Karger AG, Basel.

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Year:  2012        PMID: 22777069     DOI: 10.1159/000339029

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  4 in total

Review 1.  Lipid metabolites and their differential pro-arrhythmic profiles: of importance in the development of a new anti-arrhythmic pharmacology.

Authors:  Yangzhen Shao; Bjorn Redfors; David Benoist; Sigfus Gizurarson; Elmir Omerovic
Journal:  Mol Cell Biochem       Date:  2014-04-27       Impact factor: 3.396

2.  TMEM43 mutation p.S358L alters intercalated disc protein expression and reduces conduction velocity in arrhythmogenic right ventricular cardiomyopathy.

Authors:  Vinayakumar Siragam; Xuezhi Cui; Stephane Masse; Cameron Ackerley; Shabana Aafaqi; Linn Strandberg; Michael Tropak; Michael D Fridman; Kumaraswamy Nanthakumar; Jun Liu; Yu Sun; Bin Su; Caroline Wang; Xiaoru Liu; Yuqing Yan; Ariel Mendlowitz; Robert M Hamilton
Journal:  PLoS One       Date:  2014-10-24       Impact factor: 3.240

3.  Common lipid features of lethal ventricular tarchyarrhythmias (LVTAs) induced by myocardial infarction and myocardial ion channel diseases.

Authors:  Jiayan Wu; Qian Wu; Dian Wang; Jing Kong; Wentao Dai; Xingxing Wang; Xiaojun Yu
Journal:  Sci Rep       Date:  2017-06-26       Impact factor: 4.379

4.  Trigger-Specific Remodeling of KCa2 Potassium Channels in Models of Atrial Fibrillation.

Authors:  Ann-Kathrin Rahm; Dominik Gramlich; Teresa Wieder; Mara Elena Müller; Axel Schoeffel; Fadwa A El Tahry; Patrick Most; Tanja Heimberger; Steffi Sandke; Tanja Weis; Nina D Ullrich; Thomas Korff; Patrick Lugenbiel; Hugo A Katus; Dierk Thomas
Journal:  Pharmgenomics Pers Med       Date:  2021-05-20
  4 in total

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