Abstract
Atrial fibrillation (AF) is a common cardiac arrhythmia, which is associated with increased cardiovascular morbidity and mortality. microRNA (miRNA/miR)‑122 has been reported to be related with heart diseases, however, the functional role of miR‑122 in atrial fibrillation is unclear. Therefore, the aim of the present study was to investigate the roles of miR‑122 in atrial fibrillation. Male C57BL/6 mice were divided into the following three groups: Control, sham‑operation and AF. Mice in the AF group received transesophageal rapid atrial stimulation for the induction of AF. Cardiomyocytes isolated from mice in the AF group and were transfected with miR‑122 inhibitors. Reverse transcription‑quantitative polymerase chain reaction was used to assess the expression of miR‑122 in cardiomyocytes isolated from mice in the AF, sham‑operation and control groups, and in cells transfected with miR‑122 inhibitors. MTT and TUNEL assays were used to evaluate cardiomyocyte viability and apoptosis, respectively. Western blot analysis was used to assess the expression levels of extracellular signal‑regulated kinase (ERK) and phosphorylated (p)‑ERK, as well as the apoptosis‑associated proteins caspase‑3 and B‑cell lymphoma 2‑like 1 (Bcl‑x). The present results demonstrated that miR‑122 expression in the AF group was significantly increased compared with the sham‑operation and control groups, whereas it was significantly decreased following transfection with the miR‑122 inhibitor. Cardiomyocyte viability was increased and their apoptosis rate was significantly decreased following miR‑122 transfection. In addition, the expression of the anti‑apoptotic protein Bcl‑x was significantly upregulated, whereas the expression of the pro‑apoptotic caspase‑3 was significantly downregulated following miR‑122 inhibition. Furthermore, the p‑ERK/total ERK ratio was significantly increased in the miR‑122 inhibitor group compared with the AF and control groups. The present results suggested that miR‑122 may be implicated in the molecular mechanisms underlying the proliferation and apoptosis of cardiomyocytes in AF.