Abstract
Purpose Studies have found that microRNAs (miRNAs) are closely associated with atrial fibrillation, but their specific mechanism remains unclear. The purpose of this experiment is to explore the function of miR-29b-3p in regulating atrial remodeling by targeting PDGF-B signaling pathway and thereby also explore the potential mechanisms. Methods We randomly divided twenty-four rats into four groups. Caudal intravenous injections of angiotensin-II (Ang-II) were administered to establish atrial fibrosis models. Expressions of miR-29b-3p and PDGF-B were then tested via RT-PCR, western blot, and immunohistochemistry. Binding sites were then analyzed via the bioinformatics online software TargetScan and verified by Luciferase Reporter. We used Masson staining to detect the degree of atrial fibrosis, while immunofluorescence and western blot were used to detect the expressions of Collagen-I and a-SMA. We used immunohistochemistry and western blot to detect the expression of connexin 43 (Cx43). Results In comparison with the Ang-II group, miR-29b-3p was seen to lower the degree of atrial fibrosis, decrease the expression of fibrosis markers such as Collagen-I and a-SMA, and increase the protein expression of Cx43. MiR-29b-3p can lower the expression of PDGF-B, while the Luciferase Reporter showed that PDGF-B is the verified target gene of miR-29b-3p. Conclusions MiR-29b-3p was able to reduce atrial structural and electrical remodeling in the study's rat fibrosis model. This biological function may be expressed through the targeted regulation of the PDGF-B signaling pathway.
Highlights
The prevalence of atrial fibrillation (AF) increases with age and concomitant heart diseases
In order to further observe the biological function of miR-29b3p, a target gene was predicted by TargetScan bioinformatics online software, and this suggested that Platelet-derived growth factors (PDGF)-B is its potential target gene
The subsequent Luciferase Reporter testing showed that the expression of WT miR-29b-3p decreased in comparison with MT miR-29b-3p. This further suggested that PDGF-B is a target gene of miR-29b-3p and that miR29b-3p has a significant inhibitory effect on it, as shown in Figures 1(b) and 1(c)
Summary
The prevalence of atrial fibrillation (AF) increases with age and concomitant heart diseases. Studying new mechanisms associated with AF is critical towards finding new, more efficacious treatment methods. The pathophysiological mechanisms of AF are extremely complex, and its specific pathogenesis has yet to be fully understood, but atrial structural remodeling and electrical remodeling have been proven to contribute to the onset and maintenance of AF [4]. Atrial fibrosis plays a critical function in atrial structural remodeling and is a signature change of such remodeling. Other studies have shown that atrial electrical remodeling is believed to play an important function in the onset and maintenance of AF [6, 7]. Connexin 43(Cx43) is the primary GJP in myocardial tissue and plays an important function in the electrical connection
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