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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  miR-190a-5p  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  in situ  hybridization indicated that the expression of IL-2 in the cardiac tissues of patients with AF to be upregulated and that  miR-190a-5p  to be downregulated. Luciferase reporter assay, quantitative real-time-PCR, and whole-cell patch-clamp experiments confirmed the downregulation of IL-2 by  miR-190a-5p  and influence of the latter on the sodium current of SCN3B. Overall,  miR-190a-5p  suppressed the increase in SCN3B sodium current caused by endogenous IL-2, whereas  miR-190a-5p  inhibitor significantly reversed this effect. IL-2 was demonstrated to be directly regulated by  miR-190a-5p . We, therefore, concluded that the  miR-190a-5p /IL-2/SCN3B pathway could be involved in the pathogenesis of CAs and  miR-190a-5p  might acts as a potential protective factor in pathogenesis of CAs.

miR-190a-5p Partially Represses the Abnormal Electrical Activity of SCN3B in Cardiac Arrhythmias by Downregulation of IL-2