MiR-138-5p is downregulated in patients with atrial fibrillation and reverses cardiac fibrotic remodeling via repressing CYP11B2.

OBJECTIVE

To investigate the connection between atrial fibrillation (AF) and miR-138-5p and to further explore the possible mechanism.

PATIENTS AND METHODS

MiR-138-5p expression of right atrial appendage (RAA) tissues in 28 patients with AF and 22 patients with sinus rhythm (SR) was detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Moreover, cell proliferation assay was conducted in AC16 cells which were transfected by miR-138-5p inhibitors or mimics. Furthermore, Western blot assay, luciferase assay, and RNA immunoprecipitation assay were performed to uncover the mechanism.

RESULTS

In the present research, miR-138-5p expression in RAA samples decreased significantly in AF patients than that in SR ones. Moreover, in AC16 cells, higher miR-138-5p expression level suppressed cell growth, while cell growth was promoted after miR-138-5p was knockdown. In addition, further experiments showed that CYP11B2 acted as the main target of miR-138-5p and its expression in AF tissues negatively correlated to miR-138-5p expression.

CONCLUSIONS

All the results above elucidated that cell proliferation of AF could be inhibited by miR-138-5p via suppressing CYP11B2, which may offer a new vision for interpreting the mechanism of AF development.