MiR-23 enhances cardiac fibroblast proliferation and suppresses fibroblast apoptosis via targeting TGF-β1 in atrial fibrillation.

Objective: To investigate the specific role of miR-23 in atrial fibrillation (AF) progression and explore the possible underlying mechanism.
Patients and Methods: Right atrial appendage (RAA) tissues were collected from 30 patients with AF and 30 patients with sinus rhythm (SR), respectively. The expression level of miR-23 was detected by quantitative Real time-polymerase chain reaction (qRT-PCR). Moreover, cell counting kit-8 and flow cytometry were performed to detect the proliferation and cell apoptosis of AC16 cells after transfection with miR-23 inhibitor and mimics. Furthermore, luciferase reporter gene assay and RNA immunoprecipitation assay were performed to uncover the possible underlying mechanism.
Results: In the present study, the expression level of miR-23 in RAA tissues of AF patients was significantly higher than that of SR patients. After knockdown of miR-23 in AC16 cells, the proliferation was inhibited and cell apoptosis was induced. However, overexpression of miR-23 significantly promoted cell growth and suppressed cell apoptosis. Further experiments revealed that transforming growth factor-b1 (TGF-β1) was a direct target of miR-23. In addition, TGF-β1 expression was positively correlated with miR-23 expression in AF tissues.
Conclusions: Our findings indicated that miR-23 could promote the progression of AF via promoting TGF-β1, which might serve as a new direction for interpreting the mechanism of AF development.