MiR-30a regulates the atrial fibrillation-induced myocardial fibrosis by targeting snail 1.

Objective: Our study aims at assessing the association between miR-30a along with its target gene snail 1 and atrial fibrillation (AF)-induced myocardial fibrosis.

Methods: Ang II was used to up-regulate cardiac fibroblasts fibrosis in vitro, and then the cardiac fibroblasts were divided into the mimics group (mimics miR-30a), inhibitors group (inhibitors miR-30a), NC group (transfected miR-30a, negative control) and blank control group (non-transfected cells). Two-group (sham operated group and rapid pacing group) AF rabbit models were constructed according to whether rapid pacing was presented in the subject. Then the establishment of rabbit models was examined using histopathology after Masson staining. The mRNA and protein expression levels of snail 1 and periostin in cardiac fibroblasts and myocardial tissues were detected using the method of RT-PCR and Western blot, respectively.

Results: In vitro, our experiment showed that overexpression of miR-30a in cardiac fibroblasts contribute to a significant decrease in the average expression level of snail 1 and periostin (P < 0.05) whereas inhibition of miR-30a significantly increased the average expression level of snail 1 and periostin (P < 0.05). In vivo, the average expression level of miR-30a significantly decreased in myocardial tissues with an increased degree of myocardial fibrosis, while the snail 1 and periostin expression level significantly increased during a certain period of time (P < 0.05).

Conclusion: Our results suggest that miR-30a target snail 1 protein may be related to AF-induced myocardial fibrosis. The average expression levels of snail 1 increased significantly in both myocardial cells and tissues, while miR-30a could inhibit the expression of snail 1. Thus, we speculate that miR-30a and snail 1 may be potential therapeutic targets for curing AF-induced myocardial fibrosis.