The present study was designed to investigate whether microRNAs (miRNAs) are 
involved in atrioventricular block (AVB) in the setting of myocardial ischemia 
(MI). A cardiac-specific miR-1 transgenic (Tg) mouse model was successfully 
established for the first time in this study using microinjection. miR-1 level 
was measured by real-time qRT-PCR. Whole-cell patch clamp was employed to record 
L-type calcium current (I Ca,L) and inward rectifier K(+) current (I K1). 
Expression of connexin 43 (Cx43) protein was determined by western blot 
analysis. Alternations of [Ca(2+)]i was detected by laser scanning confocal 
microscopy in ventricular myocytes. The incidence of AVB was higher in miR-1 Tg 
mice than that in wild-type (WT) mice. The normalized peak current amplitude of 
I Ca,L was lower in ventricular myocytes from miR-1 Tg mice as compared with WT 
mice. Similarly, the current density of I K1 was decreased in miR-1 Tg mice than 
that in WT mice. Compared with WT mice, miR-1 Tg mice exhibited a significant 
decrease of the systolic [Ca(2+)]i in ventricular myocytes but a prominent 
increase of the resting [Ca(2+)]i. Moreover, Cx43 protein was downregulated in 
miR-1 Tg mice compared to that in WT mice. Administration of LNA-modified 
antimiR-1 reversed all the above changes. miR-1 overexpression may contribute to 
the increased susceptibility of the heart to AVB, which provides us novel 
insights into the molecular mechanisms underlying ischemic cardiac arrhythmias.