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46ba2c7a-caba-40a8-b777-9be44b55fddc - samples

ABSTRACT: 64 left atrial appendages from patients without atrial fibrillation (AF) undergoing cardiac surgery, patients with paroxysmal AF and with persistent AF (~20 per group). Trizol RNA isolation, rRNA depletion, paired transcriptome sequencing on illumina NovaSeq 6000. Provided are FastQ and BAM files. Additional data (e.g. clinical characteristics, RIN values etc.) can be provided upon reasonable request. The same RNA samples (62 out of 64) were used for miRNA sequencing. Results from miRNA seuqencing are stored in the EGA database managed by the same DAC.

PROVIDER: EGAD00001007693 | EGA |

REPOSITORIES: EGA

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99829f01-61af-46bf-84bb-22837c488398 - samples

Project description:64 left atrial appendages from patients without atrial fibrillation (AF) undergoing cardiac surgery, patients with paroxysmal AF and with persistent AF (~20 per group). Trizol RNA isolation, size selection, single end miRNA sequencing on 4 lanes of illumina NextSeq 500. Provided are FastQ files, one per lane per sample. Additional data (e.g. clinical characteristics, RIN values etc.) can be provided upon request. The same RNA samples (62) were used for transcriptome sequencing. Results from transcriptome sequencing are stored in the EGA database and are managed by the same DAC.

| EGAD00001007694 | EGA

Comparison of atrial appendage tissues of patients with Valvular Heart Disease and patients with Valvular Heart Disease-Atrial Fibrillation

Project description:Atrial fibrillation (AF) is the most common heart arrhythmia disease. The greatest risk of atrial fibrillation is stroke, and stroke caused by valvular heart disease with atrial fibrillation (AF-VHD) is more serious. the development mechanism from VHD to AF-VHD is not yet clear. The research on expression profiles of lncRNA and mRNA is helpful to explore molecular mechanism in patients with valvular heart disease who develop atrial fibrillation.

2018-04-12 | GSE113013 | GEO

Changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease: proteomics in human in left appendage tissue

Project description:Atrial fibrillation (AF) is the most common persistent arrhythmia that affect 1–2% of the general population. People with AF display an array of complications cardiogenic stroke and systemic embolism caused by hemodynamic instability and blood hypercoagulability in clinical practice. However, it’s still unclear whether and how ubiquitylated proteins react to AF in the left atrial appendage of patients with AF and valvular heart disease. This theory focuses on the changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease. We firstly widely analysis the proteins ubiquitination in patients with atrial fibrillation.

2021-12-24 | PXD030397 | Pride

The integrative regulatory network of circRNA, microRNA and mRNA in atrial fibrillation

Project description:Atrial fibrillation (AF) is the most common irregular heart rhythm which influence approximately 1–2% of the general population. As a potential factor for ischemic stroke, AF could also cause heart failure. The mechanisms behind AF pathogenesis are complex and remains elusive. As a new category of non-coding RNAs (ncRNAs), circular RNAs (circRNAs) have been known as the key of developmental processes, regulation of cell function, pathogenesis of heart diseases and pathological responses which could provide novel sight into the pathogenesis of AF. circRNAs function as modulators of microRNAs in cardiac disease. To investigate the regulatory mechanism of circRNA in atrial fibrillation, especially the complex interactions among circRNA, microRNA and mRNA, we collected the heart tissues from three AF patients and three healthy controls and profiled their circRNA expressions with circRNA Microarray. The differentially expressed circRNAs were identified and the biological functions of their interaction microRNAs and mRNAs were analyzed. Our results provided novel insights of the circRNA roles in atrial fibrillation and proposed highly possible interaction mechanisms among circRNAs, microRNAs and mRNAs.

2019-04-06 | GSE129409 | GEO

Atrial fibrillation is associated with altered left-to-right atria gene expression ratio: implications for arrhythmogenesis and thrombogenesis

Project description:Background: Atrial fibrillation (AF) causes atrial remodeling, and the left atrium (LA) is the favored substrate for maintaining AF. However, it remains unclear if AF remodels both atria differently and contributes to LA arrhythmogenesis and thrombogenesis. Results: AF was associated with differential LA-to-RA gene expression related to specific ion channels and pathways as well as upregulation of thrombogenesis-related genes in the LA appendage. Targeting the molecular mechanisms underlying the LA-to-RA difference and AF-related remodeling in the LA appendage may help provide new therapeutic options in treating AF and preventing thromboembolism in AF. Paired left atrial and right atrial specimens were obtained from 13 patients with persistent AF receiving valvular surgery. The Paired specimens were sent for microarray comparison. Selected results were validated by quantitative real time-PCR (q-PCR) and Western blotting. Ultrastructural changes in the atria were evaluated by immunohistochemistry.

2016-08-09 | E-GEOD-79768 | biostudies-arrayexpress

Characterizing the global changes in miRNA expression in human atrial appendages with persistent atrial fibrillation.

Project description:Atrial fibrillation (AF), the most common cardiac rhythm disorder, is a major cause of cardiovascular morbidity and mortality. AF is characterized by the rapid and irregular activation of the atrium with diverse abnormalities, including electrical, structural, metabolic, neurohormonal, or molecular alterations.3 Although the pathophysiology of AF is complex, it has traditionally been treated with antiarrhythmic drugs that control the rhythm by altering cardiac electrical properties, principally by modulating ion channel function. However, treatments of AF with antiarrhythmic drugs have mostly failed to control the heart rhythm, because the electrical characteristics of atrial cardiomyocytes are eventually altered or remodeled during the course of AF. The aims of this study were to characterize the global changes in miRNA expression in human atrial appendages and to identify the target ion channel(s) responsible for electrical remodeling in AF. In this study, we performed a comprehensive analysis of miRNA microarrays, using a strict selection for human samples.

2017-04-25 | GSE68475 | GEO

Regional specific changes in cardiac resident 1 macrophages and 2 fibroblasts modulate long-term atrial fibrillation maintenance

Project description:Most of the mechanistic insights into atrial fibrillation (AF) pathophysiology have been reported on cardiomyocytes, and it is commonly assumed that such apply in the same manner to the atria as a whole. This study shows that atrial remodeling during persistent AF (PsAF) underlies differential adaptative changes in non-myocyte populations, which depend on the functional relevance of individual-specific atrial regions to drive the overall arrhythmia. Radiofrequency delivery at driver regions can terminate the arrhythmia in pigs and achieve long-term arrhythmia AF-free survival in patients. Importantly, driver regions show overt compositional shifts in fibroblasts and myeloid populations that are highly consistent across pig models and patients. More specifically, driver regions underlie a phenotypic shift towards cardiac resident macrophages with an associated transcriptomic and proteomic profile favoring cardiomyocyte homeostasis and cell survival within a substrate prone to reentry. In fibroblasts, PTX3 represented a transcriptional hallmark exclusively present in driver regions, which supports their role on modulating the immune response of the surrounding tissue.

2025-11-06 | E-MTAB-14275 | biostudies-arrayexpress

Integrated Analysis of Dysregulated lncRNA and mRNA Expression profiles of myocardial sleevesof pulmonary veins in atrial fibrillation

Project description:Atrial fibrillation (AF) is currently the most prevalent arrhythmia worldwide.Recent clinical data implicate the additional contribution of non-coding RNAs in the pathogenesis of AFï¼which include microRNAs(miRNAs), endogenous small interfering RNAs, PIWIinteracting RNAs, and lncRNA. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with AF has not been reported. In the present study, we conducted an integrated analysis of dysregulated lncRNA and mRNA expression profiles in myocardial sleevesof pulmonary veins between the patients who develop AF and the patients who were in normal sinus rhythm, which was performed using a second generation lncRNA microarrayï¼focusing specifically on the identification and characterization of lncRNAs and mRNA potentially involving in maintaining atrial fibrillation. We conducted an integrated analysis of myocardial sleeves of pulmonary veinsï¼PVsï¼from 12 patients (6 non-AF and 6AF) in our center, of which hypertension, diabetes, smoking and alcohol abuse were excluded, using a second generation lncRNA microarray

2016-01-16 | E-GEOD-76899 | biostudies-arrayexpress

Rac1-Induced Connective Tissue Growth Factor regulates Connexin 43 and N-Cadherin Expression in Atrial Fibrillation

Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling. Array design study consists of 5 Atrial Fibrillation patients and matched 5 samples of patients in sinus rhythm (controls).

2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress

Profiling of long non-coding RNAs associated with atrial fibrillation in patients with rheumatic heart valvular disease

Project description:To investigate the expression profiles of long non-coding RNAs (lncRNAs) in atrial fibrillation (AF), atrial tissues from 5 AF patients and 5 non-AF patients that were collected for lncRNA expression microarray analyses to explore the role of lncRNA in the pathogenesis of AF.rhythm (SR) patients with rheumatic heart valvular disease,we have employed

2018-01-03 | GSE108660 | GEO

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