scholarly journals Increased α-Actinin-2 Expression in the Atrial Myocardium of Patients with Atrial Fibrillation Related to Rheumatic Heart Disease

Cardiology ◽  
2016 ◽  
Vol 135 (3) ◽  
pp. 151-159 ◽  
Author(s):  
Lei Zhang ◽  
Nan Zhang ◽  
Xuejiao Tang ◽  
Fajin Liu ◽  
Suxin Luo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Collagen Content ◽  
Atrial Fibrosis ◽  
Smad Pathway ◽  
Smad Signaling Pathway ◽  
Tgf Β1 ◽  
Rheumatic Heart

Objectives: Atrial fibrosis, a marker of atrial structural remodeling, plays a critical role in atrial fibrillation (AF). α- Actinin-2 is associated with structural remodeling related to stretching. The transforming growth factor-β1 (TGF-β1)/Smad pathway plays an important role in atrial fibrosis. We investigated the effects of the TGF-β1/Smad signaling pathway on α-actinin-2 in atrial fibrosis in patients with AF. Methods: Forty-one right atrial specimens obtained from patients with rheumatic heart disease (RHD) were divided into a chronic (c)AF group, i.e. RHD + cAF (n = 29), and a sinus rhythm group, i.e. RHD + sinus rhythm (n = 12). Patients with congenital heart disease (CHD) and sinus rhythm who underwent heart surgery served as controls (n = 10). Fibrosis was assessed by histological examination, and expression of α-actinin-2, TGF-β1 and Smad2/phosphorylated Smad2 (p-Smad2) was evaluated by immunohistochemistry, quantitative real-time PCR and Western blotting. In rat atrial fibroblasts treated with TGF-β1, the collagen content was measured using hydroxyproline detection, and α-actinin-2 and p-Smad2 were evaluated by semiquantitative reverse-transcription PCR and Western blotting. Results: The histology results revealed a significant increase in atrial fibrosis in AF patients. The collagen content, mRNA and protein expression levels of α-actinin-2 and the components of the TGF-β1/Smad signaling pathway were significantly gradually increased in the CHD + sinus rhythm, RHD + sinus rhythm and RHD + cAF groups (p < 0.05). The mRNA and protein levels of α-actinin-2 and TGF-β1 in RHD patients were positively correlated with the collagen volume fraction. A positive correlation between the expression of α-actinin-2 and TGF-β1 was also observed. In rat atrial fibroblasts treated with TGF-β1, the collagen content was greater than that in the control group (p < 0.05), and the expression levels of α- actinin-2 and p-Smad2 were also upregulated (p < 0.05). Conclusions: α-Actinin-2 expression was increased in the atrial tissues of patients with AF secondary to RHD. α-Actinin-2 was upregulated via the TGF-β1/Smad pathway in atrial fibroblasts, which suggests that it may be involved in TGF-β1/Smad pathway-induced atrial fibrosis in patients with AF.

Galectin-3 Induces Atrial Fibrosis by Activating the TGF-β1/Smad Pathway in Patients with Atrial Fibrillation

Cardiology ◽  
2020 ◽  
Vol 145 (7) ◽  
pp. 446-455 ◽  
Author(s):  
Minghan Xiao ◽  
Meixia Zhang ◽  
Mengjun Bie ◽  
Xiaowen Wang ◽  
Jingwen Guo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Atrial Fibrosis ◽  
Smad Pathway ◽  
Galectin 3 ◽  
The Relationship ◽  
Tgf Β1 ◽  
Rheumatic Heart

Background: Atrial fibrosis plays a critical role in the occurrence and maintenance of atrial fibrillation. The role of TGF-β1 in mediating atrial fibrosis is well documented. The β-galactoside-binding lectin galectin-3 (Gal-3) is mainly produced by macrophages in biological events such as inflammation and angiogenesis. Previous studies have shown that Gal-3 is associated with atrial fibrosis, but the relationship between TGF-β1 and Gal-3 in atrial fibrosis remains unclear. Objective: To determine whether Gal-3 induces atrial fibrosis and atrial fibrillation by activating the TGF-β1/Smad pathway and whether the expression of Gal-3 is mediated by TGF-β1, which can enable assessing the relationship between Gal-3 and TGF-β1 in atrial fibrosis. Methods: In this study, 30 patients’ right atrial appendages were collected and divided into 3 groups: congenital heart disease sinus rhythm group (n = 10, as a control group), rheumatic heart disease sinus rhythm group (n = 10), and rheumatic heart disease atrial fibrillation group (n = 10). Rat atrial fibroblasts were cultured in vitro, and recombinant Gal-3 and recombinant TGF-β1 proteins were added to the cell culture. The expression of Gal-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 stain to evaluate the extent of atrial fibrosis. The expression of Gal-3 and TGF-β1 was detected by immunohistochemical staining and immunofluorescence staining. Gal-3 and TGF-β1 interaction was demonstrated by immunoprecipitation. Results: The expression levels of Gal-3, TGF-β1, Smad2, and collagen I were elevated in the rheumatic heart disease atrial fibrillation group compared with the congenital heart disease sinus rhythm group and the rheumatic heart disease sinus rhythm group. In cultured atrial fibroblasts, there is a synergistic interaction between Gal-3 and TGF-β1. Gal-3 stimulated the TGF-β1/Smad pathway, and overexpression of TGF-β1 induced Gal-3 expression. Conclusions: Gal-3 and TGF-β1 interact with each other and stimulate the downstream TGF-β1/Smad pathway. This finding suggests that Gal-3 could be an important factor in TGF-β1-induced fibrosis in atrial fibrillation.

TGF-β1 and TIMP-4 regulate atrial fibrosis in atrial fibrillation secondary to rheumatic heart disease

2015 ◽  
Vol 406 (1-2) ◽  
pp. 131-138 ◽  
Author(s):  
Yu Sun ◽  
Zi-Yang Huang ◽  
Zhen-Hua Wang ◽  
Cui-Ping Li ◽  
Xian-Liang Meng ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Atrial Fibrosis ◽  
Tgf Β1 ◽  
Rheumatic Heart

scholarly journals Amiodarone in the treatment of atrial fibrillation of patients with rheumatic heart disease after valve replacement

2019 ◽  
Vol 35 (4) ◽  
Author(s):  
Kebiao Chen ◽  
Li Qin ◽  
Xin Lu ◽  
Tao Xia ◽  
Qing Gu
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Valve Replacement ◽  
Control Group ◽  
Observation Group ◽  
Maintenance Rate ◽  
Monitoring Time ◽  
Rheumatic Heart

Objectives: To explore the efficacy of amiodarone in the treatment of atrial fibrillation for patients with rheumatic heart disease after valve replacement. Methods: Eighty-six patients with rheumatic heart disease who were hospitalized between June 2016 and June 2017 and developed atrial fibrillation after valvular heart valve replacement were randomly divided into a control group and an observation group, 42 cases in each group. The control group was treated with routine medical treatment, while the observation group was given amiodarone on the basis of routine treatment. The cardiac function of the two groups were observed and recorded. Postoperative atrial fibrillation conversion rate, sinus rhythm maintenance rate, intensive care unit (ICU) monitoring time and hospital stay were compared between the two groups. Results: Compared with the control group, the improvement of cardiac function indexes of the observation group was better, and the difference was statistically significant (P<0.05). The atrial fibrillation conversion rate and the maintenance rate of sinus rhythm of the observation group were 76.2% and 47.6% respectively, which were significantly higher than 57.1% and 33.3% of the control group; the differences had statistical significance (P<0.05). The ICU monitoring time and hospitalization time of the patients in the observation group were (1.69±0.91) d and (10.24±1.11) d respectively, which were significantly shorter than (2.83±0.95) d and (14.07±1.17) d in the control group (P<0.05); the differences were statistically significant (P<0.05). Conclusion: Amiodarone can effectively treat valve replacement associated atrial fibrillation of patients with rheumatic heart disease. It can significantly improve the heart function, prevent the recurrence of atrial fibrillation, maintain sinus rhythm after operation, and shorten the time of ICU monitoring and hospitalization. doi: https://doi.org/10.12669/pjms.35.4.1298 How to cite this:Chen K, Qin L, Lu X, Xia T, Gu Q. Amiodarone in the treatment of atrial fibrillation of patients with rheumatic heart disease after valve replacement. Pak J Med Sci. 2019;35(4):---------. doi: https://doi.org/10.12669/pjms.35.4.1298 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Sign in / Sign up

Export Citation Format

Share Document