Single-cell profile of atrial human fibroblasts in cardiac arrhythmia atrial fibrillation (AF) - SmartSeq2
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PROVIDER: PRJNA624784 | ENA |
REPOSITORIES: ENA
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Project description:Atrial fibrillation (AF), the most common cardiac arrhythmia, is a major contributor to population mortality and morbidity. The goal of this study is to explore molecular mechanisms of the AF-induced profibrotic remodelling in human atrial fibroblasts (ACFs). Specifically, we assessed single-cell transcriptome of cultured human ACFs treated with calcitonin(CT) or vehicle (from 6 individual patients) and of freshly-isolated ACFs from patients with AF (4 individual patients) vs controls (4 individual patients) (SR). We found that ACF transcriptome was unaltered by CT in cultured ACFs, and identified 5 transcriptional clusters with 23 differentially expressed transcripts in AF in freshly-ioslated ACFs.
2020-07-10 | GSE148506 | GEO
Project description:Atrial fibrillation (AF), the most common cardiac arrhythmia, is a major contributor to population mortality and morbidity. The goal of this study is to explore molecular mechanisms of the AF-induced profibrotic remodelling in human atrial fibroblasts (ACFs). Specifically, we assessed single-cell transcriptome of cultured human ACFs treated with calcitonin(CT) or vehicle (from 6 individual patients) and of freshly-isolated ACFs from patients with AF (4 individual patients) vs controls (4 individual patients). We found that ACF transcriptome was unaltered by CT in cultured ACFs, and identified 5 transcriptional clusters with 23 differentially expressed transcripts in AF in freshly-ioslated ACFs.
2020-07-10 | GSE148504 | GEO
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
Project description:Atrial fibrillation (AF) is the most common sustained arrhythmia with increased risk of stroke and congestive heart failure. AF is a highly genetic heterogeneous disease, but a large proportion of AF cannot be explained by genetic variants only. Some risk factors of AF, tendentious heritable phenomenon, potentially reversible conditions and some subtypes without DNA sequence variation all indicate the participation of DNA methylation in the pathogenesis of AF. Bisulphite converted DNA from the 11 left atrium samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip GPL13534
2014-10-28 | E-GEOD-62727 | biostudies-arrayexpress
Project description:Single-cell profile of atrial human fibroblasts in cardiac arrhythmia atrial fibrillation (AF) - 10x
| PRJNA624779 | ENA
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
Project description:Atrial Fibrillation (AF), an abnormal heart rhythm characterized by the rapid and irregular beating of the atria, is the most common arrhythmia with heavy global burdens. The present project aimed to characterized the feature of metabolites in feces of AF patients by using LC-MS.
2018-12-27 | ST001208 | MetabolomicsWorkbench
Project description:Atrial fibrillation (AF) is the most common sustained arrhythmia with increased risk of stroke and congestive heart failure. AF is a highly genetic heterogeneous disease, but a large proportion of AF cannot be explained by genetic variants only. Some risk factors of AF, tendentious heritable phenomenon, potentially reversible conditions and some subtypes without DNA sequence variation all indicate the participation of DNA methylation in the pathogenesis of AF.
2014-10-28 | GSE62727 | GEO
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
Project description:Atrial fibrillation (AF) is a progressive arrhythmia for which current therapy is inadequate. During AF, rapid stimulation causes atrial remodeling that promotes further AF. The cellular signals that trigger this process remain poorly understood, however, and elucidation of these factors would likely identify new therapeutic targets. We have previously shown that immortalized mouse atrial (HL-1) myocytes subjected to 24 hr of rapid stimulation in culture undergo remodeling similar to that seen in animal models of atrial tachycardia (AT) and human AF. This preparation is devoid of confounding in vivo variables that can modulate gene expression (e.g., hemodynamics). Therefore, we investigated the transcriptional profile associated with early atrial cell remodeling. RNA was harvested from HL-1 cells cultured for 24 hr in the absence and presence of rapid stimulation and subjected to microarray analysis. Data were normalized using Robust Multichip Analysis (RMA), and genes exhibiting significant differential expression were identified using the Significance Analysis of Microarrays (SAM) method. Using this approach, 919 genes were identified that were significantly altered with rapid stimulation (763 up-regulated and 156 down-regulated). For many individual transcripts, changes typical of AF/AT were observed, with marked up-regulation of genes encoding BNP and ANP precursors, heat shock proteins, and MAP kinases, while novel signaling pathways and molecules were also identified. Both stress and survival response were evident, as well as up-regulation of multiple transcription factors. Genes were also functionally classified based on cellular component, biologic process, and molecular function using the Gene Ontology database to permit direct comparison of our data with other gene sets regulated in human AF and experimental AT. For broad categories of genes grouped by functional classification, there was striking conservation between rapidly stimulated HL-1 cells and AF/AT. Results were confirmed using real-time quantitative RT-PCR on 13 genes selected by physiological relevance in AF/AT and regulation in the microarray analysis (up, down, and nonregulated). Rapidly-stimulated atrial myocytes provide a complementary experimental paradigm to explore the initial cellular signals in AT remodeling to identify novel targets in the treatment of AF. Experiment Overall Design: HL-1 cell expression profile in vitro with and without rapid electric stimulation
2008-10-26 | E-GEOD-10598 | biostudies-arrayexpress