Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-nuclear RNA sequencing of human left atrial appendage

ABSTRACT: We herein utilized SnRNA-Seq to analyze left atrial appendage (LAA) tissues to construct a comprehensive human transcriptional profile of AF. We identified a cardiomyocyte subpopulation with high energy metabolic activity (CM_1) and an adipocyte subpopulation with a specific metabolic regulating ability (Adip_0). We also demonstrated a specific myocardial energy metabolic remodeling in AF that promoted glycolytic metabolism and inhibited mitochondrial respiratory capacity. Our results showed that epicardial adipose tissues (EAT) played a unique role in regulating this process and that cell death-inducing DFFA-like effector A (CIDEA) in EAT triggered myocardial metabolic remodeling by promoting the paracrine effects.

ORGANISM(S): Homo sapiens

PROVIDER: GSE271229 | GEO | 2025/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Spatial Transcriptomics in the Human Left Atrial Appendage and Pulmonary Vein Sleeve

Project description:Human left atrial appendage (LAA) and pulmonary vein (PV) tissues were obtained from unused lung or heart transplant donors. Paired LAA and PV sleeve tissues were obtained from two subjects, and an additional 6 PV samples were obtained from other donors. After tissue sectioning and staining, spatial RNAseq was performed. mRNAs from~1000 to 2500 genes were sequenced in each spatial area. Seurat clustering yielded 15 different clusters. These grossly split into two segregating populations, the left and right sides, with one connecting population. Multiple cells and cell types may reside in each 55 µm diameter spatial area. A clear asymmetry of clusters was observed in the PV sections, with less asymmetry in the LAA sections. Cell-type marker genes derived from human LAA single nuclei RNAseq were used to determine the dominant cell types in the 15 different clusters. The left side segregating clusters were enriched in cardiomyocytes, while the right side segregating clusters were enriched for other cell types including fibroblasts, vascular smooth muscle cells, endothelial cells, and adipocytes. Spatial transcriptomics clearly resolved the venous, cardiomyocyte, and epicardial regions of the PV tissues, as well as fibrotic regions in LAAs and PVs. Spatial expression of the AF-associated genes PITX2, SHOX2, and HCN4 was also mapped, confirming higher expression of the cardiac master transcription factor SHOX2 in the PV vs. LAA tissues. Expression of the hyperpolarization-activated ion channel HCN4 was sporadic in both PV and LAA specimens.

2026-01-05 | GSE218539 | GEO

Fibrotic Remodelling of Epicardial Adipose Tissue in Patients with Atrial Fibrillation: Comparative Analyses of Histological Findings and Computed Tomographic Imaging

Project description:Aims: We tested the hypothesis that central-marginal dispersion in adipocyte diameter in epicardial adipose tissue (EAT) would represent fibrotic remodelling of EAT, a crucial state to promote atrial myocardial fibrosis to form a substrate of atrial fibrillation (AF). We also investigated whether the central-marginal EAT density ratio by the analyses of computed tomographic (CT) imaging could predict the central-marginal adipocyte diameter ratio in EAT. Methods and results: Left atrial appendage samples were obtained from 76 consecutive AF patients during cardiovascular surgery. EAT at central area (Central EAT) and that adjacent to atrial myocardium (Marginal EAT) were evaluated. Compared to the Central EAT, the dimeter of adipocytes was smaller, fibrotic remodeling of EAT (EAT fibrosis) was more severe, and the infiltration of CD3-, CD68-, or α-SMA-positive cells were more abundant in the Marginal EAT. EAT fibrosis positively correlated with adipocyte diameter in the Central EAT, while it negatively correlated with that in the Marginal EAT, resulting in the tightly positive correlation between EAT fibrosis and the ratio of central to marginal adipocyte diameter (C/M diameter ratio) (r=0.73, p<0.01). The C/M diameter ratio was greater in patients with persistent AF (PeAF) than in those with paroxysmal AF (PAF) (p<0.01). The CT density in Central EAT and Marginal EAT was measured and their ratio (C/M density ratio) was calculated. The C/M density ratio correlated tightly with the C/M diameter ratio (r=0.69, p<0.01). Conclusion: Our results suggest that C/M adipocyte diameter ratio was associated with fibrotic remodeling of EAT and progression of AF. Our results also suggest that C/M adipocyte diameter ratio could be accurately predicted by the analyses of CT findings noninvasively.

2021-08-25 | GSE154436 | GEO

Reduced left atrial cardiomyocyte PITX2 and elevated circulating BMP10 predict atrial fibrillation after ablation

Project description:Background: Genomic and experimental studies suggest a role for PITX2 in atrial fibrillation (AF). To assess whether this association is relevant for recurrent AF in patients, we tested whether left atrial PITX2 affects recurrent AF after AF ablation. Methods: mRNA concentrations of PITX2 and its cardiac isoform, PITX2c, were quantified in left atrial appendages (LAA) from patients undergoing thoracoscopic AF ablation, either in whole LAA tissue (n=83) or in LAA cardiomyocytes (n=52), and combined with clinical parameters to predict AF recurrence. Literature suggests bone morphogenetic protein 10 (BMP10) as a PITX2-repressed, atrial-specific, secreted protein. BMP10 plasma concentrations were combined with eleven cardiovascular biomarkers and clinical parameters to predict recurrent AF after catheter ablation in 359 patients. Results: Reduced cardiomyocyte PITX2 concentrations, but not whole LAA tissue PITX2, were associated with AF recurrence after thoracoscopic AF ablation (16% decreased recurrence per 2-(ΔΔCt) increase in PITX2). RNA sequencing, qPCR and Western blotting confirmed BMP10 as one of most PITX2-repressed atrial genes. Left atrial size (hazard ratio per mm increase, HR [95%CI] 1.055 [1.028, 1.082], non-paroxysmal AF (HR 1.672 [1.206, 2.318]) and elevated BMP10 (HR 1.339 [CI 1.159, 1.546] per quartile increase) were predictive of recurrent AF. BMP10 outperformed eleven other cardiovascular biomarkers in predicting recurrent AF. Conclusions: Reduced left atrial cardiomyocyte PITX2 and elevated plasma concentrations of the PITX2-repressed, secreted, atrial protein BMP10 identify patients at risk of recurrent AF after ablation.

2020-06-19 | GSE152181 | GEO

Atrial fibrillation variant-to-gene prioritization through cross-ancestry eQTL and single-nucleus multiomic analyses (bulk RNA-seq)

Project description:Atrial fibrillation (AF) is the most common arrhythmia in the world, and is linked to significant morbidity and mortality. Despite advances in the treatment and management of AF, important challenges remain for patients. Human genetics can provide strong therapeutic candidates, but the identification of the causal genes and their functions is difficult. Here, we apply an AF fine-mapping strategy that leverages results from a cross-ancestry genome-wide association study (GWAS), expression quantitative trait loci (eQTLs) from left atrial appendages (LAA) obtained from two cohorts with distinct ancestry (European and East Asian), and a paired RNAseq and ATACseq LAA single-nucleus assay (sn-multiome). We found that AF-associated LAA eQTLs are largely consistent across ancestries. At ten AF loci, our co-localization and fine-mapping analyses implicated 14 genes. Furthermore, by integrating our LAA sn-multiome data and other epigenomic datasets with our fine-mapping results, we identified four primary candidate causal AF variants, including rs7612445 at GNB4 and rs242557 at MAPT, for which we propose molecular mechanisms of AF-association at the cellular level. Finally, we showed that the repression of the strongest AF-associated eQTL gene, LINC01629, in human embryonic stem cell-derived cardiomyocytes using CRISPR inhibition results in the dysregulation of pathways linked to genes involved in the development of atrial tissue and the cardiac conduction system (e.g. HCN4, PITX2 and TBX5).

2024-07-09 | GSE271839 | GEO

Atrial fibrillation variant-to-gene prioritization through cross-ancestry eQTL and single-nucleus multiomic analyses

2024-07-09 | GSE238242 | GEO

Dynamic Enlargement and Mobilization of Lipid Droplets in Pluripotent Cells Coordinate Morphogenesis during Mouse Peri-implantation Development

Project description:ESCs grown in Growth Factor-reduced Matrigel can recapitulate in vitro the morphogenesis of the epiblast tissue during peri-implantation development. We performed RNA-sequencing on wild-type (WT) and Cidea knockout (KO) mouse R1-ESCs grown under self-renewing (serum/LIF) conditions and in 3D culture conditions (i.e., 3D spheroids ) at different time-points of differentiation (24h and 48h post-induction) to help us understand the role of the lipid droplet associated factor CIDEA (Cell Death Inducing DFFA Like Effector A) in ESC biology and during the process of morphogenesis.

2022-05-16 | GSE165563 | GEO

Region-specific gene expression profiles in left atria of patients with valvular atrial fibrillation

Project description:Of 54,675 expressed sequence tags, microarray analysis revealed that 391 genes were differently expressed (>1.5-fold difference) between LA-PV junction and LAA, including genes related to arrhythmia, cell death, fibrosis, hypertrophy, and inflammation. Microarray and q-PCR produced parallel results in analyzing the expression of particular genes. The expression of paired like homeodomain-2 (PITX2) and its target protein (short stature homeobox-2 [SHOX2]) was greater in LA-PV junction than in LAA, which may contribute to arrhythmogenesis. Five genes related to thrombogenesis were up-regulated in LAA, which may implicate for the preferential thrombus formation in LAA. Genes related to fibrosis were highly expressed in LAA, which was reflected by intense ultrastructural changes in this region Paired LA-PV junction and left atrial appendage (LAA) specimens were obtained from 16 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.

2013-09-18 | E-GEOD-41177 | biostudies-arrayexpress

Extracellular vesicles from epicardial fat mediate long-distance heart-brain communication and promote atrial fibrillation associated cognitive impairment (EAT exosomal miRNA-seq and hippocampal mRNA-seq)

Project description:2 weeks of rapid atrial pacing increased the release of epicardial adipose tissue (EAT) exosomes. The red fluorescence of Ad-CD63-RFP traces the increase of EAT exosomes in the canine hippocampus. RNA Sequencing showed that the differentially expressed genes of cfa-miR-22e in EAT exosomes were significantly increased, and its target gene of IL33 was down-regulated in the hippocampus. Exosomes secreted by EAT in AF model canine penetrate the BBB, and activate hippocampal microglia through cfa-miR-22e/IL33 signaling pathway, which may be related to the increased risk of cognitive impairment in AF.

2024-05-01 | GSE240776 | GEO

RNA-sequencing of epicardial adipose tissue of patients with atrial fibrillation

Project description:Accumulating studies have suggested that epicardial adipose tissue play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying non-coding RNAs, may modulate atrial remodeling. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with AF.

2019-08-07 | GSE135445 | GEO

Microsecond pulsed electric fields induce myocardial ablation by damaging mitochondria

Project description:Catheter ablation is an effective treatment to prevent recurrence of Atrial fibrillation (AF) and can be used to maintain sinus rhythm and improve symptoms of AF, but to some extent it can cause a range of adverse effects associated with catheter ablation. Pulsed electric field is a newer treatment modality to replace catheter ablation for atrial fibrillation due to its fewer side effects. Different from radiofrequency ablation, which destroys diseased myocardial tissue by thermal energy, pulsed electric field ablation achieves the purpose of atrial fibrillation ablation by inducing damage to diseased myocardial cells through irreversible electroporation. However, some experimental parameters and mechanism of pulsed electric fields remain unclear.

2023-11-30 | GSE214387 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data