| Background:Atrial fibrosis plays a critical role in the occurrence and maintenance of atrial fibrillation.It activates the downstream TGF-β1/Smad pathway and leads to the development of atrial fibrillation.Theβ-galactoside-binding lectin galectin-3(Galectin-3)is mainly produced by macrophages in biological events such as inflammation and angiogenesis.Previous studies have shown that serum Galectin-3 levels are associated with atrial fibrillation,but the molecular mechanisms of this association remain unclear.Methods: In this study,patients’ right atrial appendages were collected,and the expression of Galectin-3,TGF-β1,Smad2,and collagen I was detected by western blotting and quantitative real-time PCR.Atrial tissues were stained with Masson’s trichrome to evaluate atrial fibrosis.The expression of Galectin-3 and TGF-β1 was detected by immunohistochemical staining.Rat atrial fibroblasts were cultured in vitro,and recombinant Galectin-3 protein was added to the cell culture.The expression of TGF-β1,Smad2,and collagen I was detected by western blotting and quantitative real-time PCR.Results:Galectin-3 is involved in human and rat atrial fibrosis.In the patient’s atrial tissue,we found that Galectin-3 is expressed in the human right atrial appendages,and patients with rheumatic heart disease with atrial fibrillation have higher level of atrial fibrosis and higher expression levels of Galectin-3,TGF-β1,Smad2,and collagen I than patients withcongenital heart disease with sinus rhythm and those with rheumatic heart disease with sinus rhythm.In cultured atrial fibroblasts,Galectin-3stimulated the expression of TGF-β1,Smad2,and collagen I.Conculsions:Galectin-3 is expressed in the human right atrial appendages and may be a potential upstream molecule of the TGF-β1/Smad pathway in human atrial and rat atrial fibroblasts.This suggests that Galectin-3 is a potential regulator of atrial fibrosis induced by the TGF-β1/Smad pathway in patients with atrial fibrillation. |
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