Partially Represses the Abnormal Electrical Activity of SCN3B in Cardiac Arrhythmias by Downregulation of IL-2.

Cardiac arrhythmias (CAs) are generally caused by disruption of the cardiac conduction system; interleukin-2 (IL-2) is a key player in the pathological process of CAs. This study aimed to investigate the molecular mechanism underlying the regulation of IL-2 and the sodium channel current of sodium voltage-gated channel beta subunit 3 (SCN3B) by in the progression of CAs. ELISA results suggested the concentration of peripheral blood serum IL-2 in patients with atrial fibrillation (AF) to be increased compared to that in normal controls; fluorescence hybridization indicated that the expression of IL-2 in the cardiac tissues of patients with AF to be upregulated and that to be downregulated. Luciferase reporter assay, quantitative real-time-PCR, and whole-cell patch-clamp experiments confirmed the downregulation of IL-2 by and influence of the latter on the sodium current of SCN3B. Overall, suppressed the increase in SCN3B sodium current caused by endogenous IL-2, whereas inhibitor significantly reversed this effect. IL-2 was demonstrated to be directly regulated by . We, therefore, concluded that the /IL-2/SCN3B pathway could be involved in the pathogenesis of CAs and might acts as a potential protective factor in pathogenesis of CAs.