Abstract
Background: The mechanism of Interleukin-17 (IL-17) induced ventricular arrhythmia (VA) remains unclear. This study aimed to investigate the effect of intracellular calcium (Cai) handling and VA susceptibility by IL-17.Methods: The electrophysiological properties of isolated perfused rabbit hearts under IL-17 (20 ng/ml, N = 6) and the IL-17 with neutralizer (0.4 μg/ml, N = 6) were evaluated using an optical mapping system. The action potential duration (APD) and Cai transient duration (CaiTD) were examined, and semiquantitative reverse transcriptase-polymerase chain reaction analysis of ion channels was performed.Results: There were longer APD80, CaiTD80 and increased thresholds of APD and CaiTD alternans, the maximum slope of APD restitution and induction of VA threshold in IL-17 group compared with those in IL-17 neutralizer and baseline groups. During ventricular fibrillation, the number of phase singularities and dominant frequency were both significantly greater in IL-17 group than in baseline group. The mRNA expressions of the Na+/Ca2+ exchanger, phospholamban, and ryanodine receptor Ca2+ release channel were upregulated, and the subunit of L-type Ca2+ current and sarcoplasmic reticulum Ca2+-ATPase 2a were significantly reduced in IL-17 group compared to baseline and IL-17 neutralizer group.Conclusions: IL-17 enhanced CaiTD and APD alternans through disturbances in calcium handling, which may increase VA susceptibility.
Highlights
Ischemic ventricular arrhythmia (VA) is strongly associated with increased inflammatory activities [1]
IL-17 enhanced Cai transient duration (CaiTD) and action potential duration (APD) alternans through disturbances in calcium handling, which may increase VA susceptibility
SD of APD80 was shorter in the IL-17 neutralizer group (P < 0.05 at pacing cycle lengths (PCL) of 300–400 ms) than in the IL-17 group (Figure 2C)
Summary
Ischemic ventricular arrhythmia (VA) is strongly associated with increased inflammatory activities [1]. Interleukin (IL), the pro-inflammatory cytokine of the newly described T helper 17 (TH 17) cell subset, has a major function in shielding the host anti extracellular pathogens, it promotes inflammation in autoimmune diseases and mediator of tissue inflammation [2, 3]. VA can be triggered through multiple electrophysiological mechanisms, including prolonged ventricular action potential duration (APD), slowed conduction, increased electrical restitution, and perturbed intracellular calcium (Cai) signaling [6, 7]. This study aimed to investigate the influence of IL-17 on Cai handling and VA susceptibility. This study aimed to investigate the effect of intracellular calcium (Cai) handling and VA susceptibility by IL-17
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