MicroRNAs (miRNAs) are increasingly reported to have important roles in diverse 
biological and pathological processes. Changes in abundance of muscle-specific 
microRNA, miR-1, have been implicated in cardiac disease, including arrhythmia 
and heart failure. However, the specific molecular targets and cellular 
mechanisms involved in the miR-1 function in the heart are only beginning to 
emerge. In this study, we investigated miR-1 expression and its potential role 
in the mouse model of viral myocarditis (VMC). The expression levels of miR-1 
and its target gene Connexin 43 (Cx43) were measured by real-time PCR and 
western blotting, respectively. The miR-1 expression levels were significantly 
increased in cardiac myocytes from VMC mice in comparison with control samples 
(relative expression: 10 ± 2.5 vs. 31 ± 7.6, P < 0.05). Among the target genes 
of miR-1, the expression Cx43 protein was significantly reduced in such mice 
while there was no significant difference in the its mRNA levels. Our results 
revealed an inverse correlation between miR-1 levels and Cx43 protein expression 
in VMC samples. Using a bioinformatics-based approach, we found two identical 
potential binding sites were found in mouse miR-1 and Cx43 3'- untranslated 
region, this confirms a possible regulatory role of miR-1. In cultured, miRNA 
transfected myocardial cells, we show overexpression of miR-1 accompanied by a 
decrease in Cx43 protein's expression. There was only a slight (not 
statistically significant) drop in Cx43 mRNA levels. Our results indicate that 
miR-1 is involved in VMC via post-transcriptional repression of Cx43, and might 
constitute potentially valuable data for the development of a new approach in 
the treatment of this disease.