Effects of the Dectin-2/TNF-α Pathway on Ventricular Arrhythmia after Acute Myocardial Infarction in Mice

Abstract

Background. Inflammatory responses are involved in ischemic injuries and cardiac repair after acute myocardial infarction (AMI). Dectin-2 is a C-type lectin receptor that induces cytokine production and promotes local inflammatory responses. Methods. Sixty C57BL/6 mice were randomly assigned to a sham-surgery group, AMI group, or AMI + etanercept group, with 20 mice in each group. Programmed electrical stimulation (PES) was used to anesthetized mice to induce ventricular tachycardia. Real-time polymerase chain reaction (PCR) and western blot analysis were adopted to determine the expression and distribution of dectin-2 in heart tissues. The tumor necrosis factor-α (TNF-α), interferon-gamma (IFN)-γ, interleukin (IL) 4, and IL-5 levels in the serum were determined using ELISAs. Results. The expression of dectin-2 and TNF-α was increased in the myocardium in AMI, and the susceptibility to ventricular arrhythmia (VA) was increased. The induction rate of VA was significantly decreased by etanercept. Compared with those in the sham-surgery group, the AMI group showed significantly higher serum TNF-α and IFN-γ levels and lower IL-4 and IL-5levels. Conclusion. Dectin-2 intensifies the activation of the TNF-α immune reaction through the Th1 differentiation, which may increase vulnerability to VA in AMI.