Similar Datasets
Project description:Effect of obesity on mouse atrial gene expression.
| PRJNA869599 | ENA
Project description:Obesity is linked to an increased risk of atrial fibrillation (AF) via increased oxidative stress. While NADPH oxidase II (NOX2), a major source of oxidative stress and reactive oxygen species (ROS) in the heart predisposes to AF, the underlying mechanisms remain unclear. Here, we studied NOX2-mediated ROS production in obesity-mediated AF using Nox2-knock-out (KO) mice and mature human induced pluripotent stem cell-derived atrial cardiomyocytes (hiPSC-aCMs). Diet-induced obesity (DIO) mice and hiPSC-aCMs treated with palmitic acid (PA) were infused with a NOX blocker (apocynin) and a NOX2-specific inhibitor, respectively. We showed that NOX2 inhibition normalized atrial action potential duration and abrogated obesity-mediated ion channel remodeling with reduced AF burden. Unbiased transcriptomics analysis revealed that NOX2 mediates atrial remodeling in obesity-mediated AF in DIO mice, PA-treated hiPSC-aCMs, and human atrial tissue from obese individuals by upregulation of paired-like homeodomain transcription factor 2 (PITX2). Furthermore, hiPSC-aCMs treated with hydrogen peroxide, a NOX2 surrogate, displayed increased PITX2 expression, establishing a mechanistic link between increased NOX2-mediated ROS production and modulation of PITX2. Our findings offer insights into possible mechanisms through which obesity triggers AF and support NOX2 inhibition as a potential novel prophylactic or adjunctive therapy for patients with obesity-mediated AF.
2024-10-09 | GSE271748 | GEO
Project description:Atrial fibrillation is associated with stuctural remodelling of the atria that involves various cell types, including cardiac myocytes, endothelial cells, and immune cells. Atrial myopathy forms the substrate for an increased risk for AF onset and on the other hand AF drives atrial myopathy. Atrial myopathy is linked to risk factors such as aging, hypertension, obesity, or heart failure. Aldosterone and the mineralocorticoid receptor are drivers of pathological remodeling in atrial myopathy. In this study, we investigated the effect of aldosterone on left atrial gene expression and cell-cell communication.
2025-02-18 | GSE289629 | GEO
Project description:Modulation of NOX2 causes Obesity- Mediated Atrial Fibrillation
| PRJNA1133029 | ENA
Project description:Effect of obesity on mouse lung transcriptome
| PRJEB57780 | ENA
Project description:We conducted RNAseq on old PKCε KO vs old WT mouse atrial samples to identify pathways contributing to reduced inducibility and duration of AF in the old KO compared to old WT mice.
2022-11-07 | GSE211472 | GEO
Project description:RNA sequencing of dissected left atrial free wall and left atrial appendage of adult New Zealand White rabbit
2018-10-19 | GSE117801 | GEO
Project description:Project description: Proteomics study of the role of nucleotide oligomerization domain type 1 (NOD1) in a mouse model of heart failure. A high-throughput quantitative proteomic analysis was performed in atrial myocardium obtained from Wt- and Nod1-/--Tac mice and their respective Sham groups.
2025-07-17 | PXD053998 | JPOST Repository
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
Project description:We generated mouse heart organoids from mouse embryonic stem cells. The heart organoids showed both atrium-like and ventricle-like morphology similar to those of embryonic hearts. Therefore we performed RNA-seq analysis to compare atrial and ventricular gene expression profiles between mouse embryonic hearts and induced heart organoids.
2020-06-30 | GSE143932 | GEO