JOURNAL ARTICLE

DACT2 regulates structural and electrical atrial remodeling in atrial fibrillation

Jian Hou, Shaojie Huang, Yan Long, Jiaxing Huang, Song Yang, Jianping Yao, Guangxian Chen, Yuan Yue, Mengya Liang, Bo Mei, Jiawen Li, Zhongkai Wu
Journal of Thoracic Disease 2020, 12 (5): 2039-2048
32642106

Background: Atrial fibrillation (AF) is the most common sustained arrhythmia. DACT2 is a novel and important mediator of signaling pathways. The aim of this study was to investigate the clinical significance and functions of DACT2 expression in AF.

Methods: Immunohistochemistry was used to detect the DACT2 expression pattern in valvular disease patients. DACT2 was overexpressed in HL-1 cells and primary atrial fibroblasts. The expression levels of the potassium channel, the L-type calcium current channel, sodium ion channel proteins and collagen proteins were detected by real-time polymerase chain reaction (RT-PCR). The proteins involved in the Wnt and TGF-β signaling pathways were detected after DACT2 overexpression by western blotting.

Results: DACT2 expression was significantly associated with AF (P=0.016). The fibrosis ratio in the strong DACT2 expression group was significantly lower than that in the weak DACT2 expression group (weak: 0.198±0.091, strong: 0.129±0.064, P=0.048), and a negative correlation between DACT2 expression levels and fibrosis severity was observed (Spearman rho =-0.476, P=0.010). DACT2 significantly increased the expression levels of KCNE5 and decreased the levels of KCNH2 and SCN5A. Overexpression of DACT2 significantly inhibited the expression of collagen I and collagen III in primary rat atrial fibroblasts. DACT2 could facilitate β-catenin accumulation by reducing its phosphorylation at Thr41/Ser45 in HL-1 cells and inhibit the TGF-β signaling pathway in primary atrial fibroblasts.

Conclusions: DACT2 played a role in AF by regulating both structural and electrical atrial remodeling and by affecting β-catenin accumulation and TGF-β signaling, and it could serve as a protective factor against AF in valvular heart disease.

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