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Electrophysiological Effects of Lysophosphatidylcholine on HL-1 Cardiomyocytes Assessed with a Microelectrode Array System

Artikel i vetenskaplig tidskrift
Författare Sigfus Gizurarson
Yangzhen Shao
Azra Miljanovic
Truls Råmunddal
Jan Borén
Lennart Bergfeldt
Elmir Omerovic
Publicerad i Cellular Physiology and Biochemistry
Volym 30
Nummer/häfte 2
Sidor 477-488
ISSN 1015-8987
Publiceringsår 2012
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 477-488
Språk en
Länkar dx.doi.org/10.1159/000339029
Ämnesord HL-1 cardiomyocytes, Lysophosphatidylcholine, Microelectrode array system, Electrophysiology, Field, cell-derived cardiomyocytes, cardiac myocytes, heart, accumulation, ischemia, lysophosphoglycerides, fibrillation, propagation, myocardium, metabolite
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

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 mu M 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 (EC50) of LPC was around 12 mu M. The beating rate and peak-peak amplitude of FP thus decreased at concentrations >= 12 mu M and were inversely proportional to increased LPC concentration. The duration of FP was significantly prolonged with LPC above 12 mu M 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 mu M. 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 (C) 2012 S Karger AG, Basel

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