miR‑132 in atrial fibrillation directly targets connective tissue growth factor.

Atrial fibrillation (AF) is the most frequently occurring, persistent cardiac arrhythmia, and the hallmark of AF‑dependent structural remodeling is atrial fibrosis. Connective tissue growth factor (CTGF) is important in the process of fibrosis. The association between miRNA and CTGF in AF‑dependent fibrosis remains to be elucidated. The present study aimed to determine if microRNA (miR)‑132 was able to regulate CTGF with an anti‑fibrotic effect in AF. A total of ten dogs or patients were assigned to control (n=4) and AF groups (n=6). The left atrium of dogs or right atrial appendage of patients was observed. Following this, cardiac fibroblasts of adult rats were treated with or without angiotensin II (Ang II). Furthermore, cardiac fibroblasts were transfected with miR‑132 mimics, inhibitor or negative control. The expression of miR‑132 and CTGF were analyzed by reverse transcription‑quantitative polymerase chain reaction or western blotting. These analyses demonstrated that miR‑132 expression was decreased and CTGF increased in the human and canine models with AF. The expression of miR‑132 and CTGF protein levels were upregulated in Ang II stimulated cardiac fibroblasts of adult rats. Furthermore, when miR‑132 was introduced into cardiac fibroblasts, the expression of miR‑132 increased significantly whereas the expression of CTGF decreased. Inverse results were observed when cardiac fibroblasts were transfected with miR‑132 inhibitor. The luciferase reporter assay was then performed to confirm that miR‑132 may suppress CTGF expression by binding to its 3'‑untranslated region. In conclusion, miR‑132 may target CTGF in regulating fibrosis in Ang II‑treated cardiac fibroblasts. These findings may aid in providing potential therapeutic targets in the treatment of AF.