Key result
Elevated miR-23 in atrial fibrillation promotes cell growth and suppresses apoptosis via targeting TGF-β1.
Why the study?
The specific role of miR-23 in atrial fibrillation progression and its underlying mechanism were not fully understood.
Does miR-23 expression affect cardiac fibroblast proliferation and apoptosis via TGF-β1 in atrial fibrillation?
Case-Control (n=60)
Does miR-23 expression affect cardiac fibroblast proliferation and apoptosis via TGF-β1 in atrial fibrillation?
miR-23 promotes the progression of atrial fibrillation by enhancing cardiac fibroblast proliferation and suppressing apoptosis via targeting TGF-β1.
miR-23 may promote AF-related fibrosis; hypothesis-generating in animal models, requiring human validation before any clinical consideration.
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.
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Rb et al. (2019) conducted a case-control in Atrial fibrillation (n=60). miR-23 vs. Sinus rhythm / miR-23 knockdown was evaluated on miR-23 expression, cell proliferation, and apoptosis. miR-23 expression was significantly higher in atrial fibrillation patients than in those with sinus rhythm, and it promoted cell growth and suppressed apoptosis by targeting TGF-β1.
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