Abstract
Viral myocarditis (VMC) is a life-threatening disease that leads to heart failure or cardiac arrhythmia. A large number of researches have revealed that mircroRNAs (miRNAs) participate in the pathological processes of VMC. We previously reported that miR-1 repressed the expression of gap junction protein α1 (GJA1) in VMC. In this study, miR-19b was found to be significantly upregulated using the microarray analysis in a mouse model of VMC, and overexpression of miR-19b led to irregular beating pattern in human cardiomyocytes derived from the induced pluripotent stem cells (hiPSCs-CMs). The upregulation of miR-19b was associated with decreased GJA1 in vivo. Furthermore, a miR-19b inhibitor increased, while its mimics suppressed the expression of GJA1 in HL-1 cells. When GJA1 was overexpressed, the miR-19b mimics-mediated irregular beating was reversed in hiPSCs-CMs. In addition, the effect of miR-19b on GJA1 was enhanced by miR-1 in a dose-dependent manner. These data suggest miR-19b contributes to irregular beating through regulation of GJA1 by cooperating with miR-1. Based on the present and our previous studies, it could be indicated that miR-19b and miR-1 might be critically involved in cardiac arrhythmia associated with VMC.
Highlights
Viral myocarditis (VMC) is a severe cardiovascular disease characterized by inflammatory infiltration in the myocardium
These results suggested that Coxsackievirus B3 (CVB3) infection triggered significant myocardial lesions, and confirming the successful establishment of VMC model in mice
The results indicated miR-19b may play an important role in murine VMC model
Summary
Viral myocarditis (VMC) is a severe cardiovascular disease characterized by inflammatory infiltration in the myocardium. It is one of the most challenging problems in cardiology, which can lead to heart failure or cardiac arrhythmia and contribute to sudden unexpected death in young and healthy individuals. VMC accounts for up to 12% of sudden deaths in patients under 40 years of age and becomes a leading cause of dilated cardiomyopathy which may result in deaths in 50% of patients 1–2 years after diagnosis [1,2,3,4]. The therapeutic interventions of CVB3-induced myocarditis remain limited and nonspecific [1]. The exact mechanisms of how CVB3-induced myocarditis are not well understood
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