scholarly journals Altered Expression of Transfer-RNA-Derived Small RNAs in Human With Rheumatic Heart Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhao-yu Yang ◽  
Peng-fei Li ◽  
Zhi-qing Li ◽  
Tao Tang ◽  
Wei Liu ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Small Rnas ◽  
Public Health Problem ◽  
Transfer Rna ◽  
Regulation Of Transcription ◽  
Altered Expression ◽  
Qrt Pcr ◽  
Rheumatic Heart

Rheumatic heart disease (RHD) remains a severe public health problem in developing countries. Atrial fibrillation (AF) is a medical complication of RHD. Although the understanding of disease pathogenesis has advanced in recent years, the key questions need to be addressed. Transfer RNA–derived small RNAs (tsRNAs) are a novel type of short non-coding RNAs with potential regulatory functions in various physiological and pathological processes. The present study used tsRNAs sequencing to investigate the relationship between RHD and atrial fibrillation (AF). Three paired cardiac papillary muscles were taken from six rheumatic RHD patients with AF (3 cases) or without AF (3 cases) from January 2016 to January 2017 in Xiangya Hospital, Central South University. A total of 219 precisely matched tsRNAs were identified, and 77 tsRNAs (fold change > 2.0 and P < 0.05) were differently changed. Three tsRNAs (AS-tDR-001269, AS-tDR-001363, AS-tDR-006049) were randomly selected and confirmed by qRT-PCR. The results of qRT-PCR were consistent with tsRNAs sequencing, suggesting the tsRNAs sequencing was reliable. Subsequently, we predicted the target mRNAs of the three tsRNAs. Moreover, we verified the functions of tsRNAs targeting mRNAs in vitro. Finally, bioinformatics analysis indicated that the target genes were abundant in regulation of transcription, DNA binding, intracellular. Most of the genes were predicted to interplay with cytokine-cytokine receptor by KEGG analysis. Our findings uncover the pathological process of AF in RHD through tsRNAs sequencing. This research provides a new perspective for future research on elucidating the mechanism of AF in RHD and offers potential new candidates for the treatment and diagnosis.

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.

scholarly journals Clinical and Etiological Profile of Patients with Atrial Fibrillation (AF): Analysis and implications

2017 ◽  
Vol 4 (1) ◽  
pp. 5-12
Author(s):  
Ram Narayan Mandal ◽  
Ajay Kumar Mishra ◽  
Elena Leonidovna Mandal
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Dilated Cardiomyopathy ◽  
Rheumatic Heart Disease ◽  
Ischemic Heart ◽  
Systemic Hypertension ◽  
Clinical Hospital ◽  
Medical College ◽  
Rheumatic Heart

Background and Objectives: Atrial fibrillation (AF) is a frequently encountered cardiac arrhythmia which may be either symptomatic or asymptomatic. So, this study was conducted to know clinical presentation and to find out possible clinical and etiological profile of patients with AF.Material and Methods: This cross sectional study was conducted at Osh Regional Integrated Clinical Hospital, Osh Territorial City Clinical Hospital, The Kyrgyz Republic in collaboration with Janaki Medical College Teaching Hospital, Janakpurdham, Nepal. Sixty consecutive patients with AF were taken. Presenting complaints, past history, personal history was recorded. A thorough clinical examination was done, electrocardiogram, chest X-Ray posterio-anterior view, echocardiogram, thyroid function test and relevant test were done and analyzed.Results: Forty percent of the patients complained palpitation. Systemic thrombo-embolism was found in 15% of the patients. Other presenting complaints were cough, chest pain, shortness of breath, dizziness, swelling of the legs, tremors. Eighteen percent of patients presented with features of congestive cardiac failure and 30% of the patients gave history of rheumatic heart disease, 16.6% and 11.6% hypertension and ischemic heart disease respectively. Etiology-wise, rheumatic heart disease was the most common (46.6%) followed by hypertension (21.6%), ischemic heart disease (11.6%), dilated cardiomyopathy (6.6%), hyperthyroidism (5%), pneumonia (5%).Conclusion: Rheumatic heart disease, especially mitral stenosis is the most common cause of AF in this study. Systemic hypertension was next common etiology of AF, followed by ischaemic heart disease, dilated cardiomyopathy, thyroid disease. Heart failure, Systemic thromboembolism, decreased exercise tolerance are a major determinants for development of significant morbidity and mortality.Janaki Medical College Journal of Medical Sciences (2016) Vol. 4 (1): 5-12

Efficacy of Surgical Ablation of Atrial Fibrillation in Patients With Rheumatic Heart Disease

2010 ◽  
Vol 89 (5) ◽  
pp. 1437-1442 ◽  
Author(s):  
Leonid Sternik ◽  
David Luria ◽  
Michael Glikson ◽  
Ateret Malachy ◽  
Maya First ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Surgical Ablation ◽  
Rheumatic Heart

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.

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