Atrial fibrosis is the hallmark of atrial fibrillation (AF) dependent structure remodeling. Besides, sprouty 1 (Spry1) plays a key role in the process of fibrosis. In this study, we investigated whether Spry1 could regulate TGF-β1 in atrial fibrosis. Ten dogs or patients were assigned to control (n=4) and AF group (n=6). The left atrium of dogs or right atrial appendage of patients was taken. After that, cardiac fibroblasts were treated with or without angiotensin II (Ang II). Furthermore, cardiac fibroblasts were transfected with lentivirus of Spry1 over-expression vector, Spry1 shRNA or negative control (NC). And the protein expression of Spry1 and TGF-β1 was analyzed by western blot and immunohistochemistry. The results showed that TGF-β1 was highly expressed while Spry1 was lowly expressed in the models of human and canine with AF. Besides, the protein expression of TGF-β1 was up-regulated and Spry1 was down-regulated in Ang II stimulated cardiac fibroblasts. Furthermore, when Spry1 was knockdown in Ang II-induced cardiac fibroblasts, the cell proliferation and the TGF-β1 protein expression increased significantly, while Spry1 over-expression showed inverse results. Our results demonstrated that Spry1 may target TGF-β1 in regulating fibrosis. These findings may provide possible therapeutic targets in atrial fibrosis.
Keywords: Angiotensin II; Atrial fibrillation; Fibrosis; Spry1; TGF-β1.
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