Gene expression in rabbit left atrial free wall and left atrial appendage
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ABSTRACT:
PROVIDER: PRJNA483207 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7612766.fastq.gz | Fastqsanger.gz | |||
| SRR7612767.fastq.gz | Fastqsanger.gz |
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Project description: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.
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Project description:Spatial Transcriptomics in the Human Left Atrial Appendage and Pulmonary Vein Sleeve
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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
Project description:Background: Chronic atrial fibrillation (AF) is a complication associated with the dilated atria of patients with valvular heart disease and contributes to worsened pathology. Methods and Results: Using microarray technology, we examined microRNA (miR) expression profiles in right and left atrial appendage tissue from valvular heart disease (VHD) patients. Right atrial appendage from patients undergoing coronary artery bypass grafting (CABG) and left atrial (LA) appendage from healthy hearts not used for transplant were used as controls. VHD induced different changes in miR expression in LA compared with right atria (RA). Fifty-two (52) miRs were altered by VHD in LA, compared with 5 in RA tissue. There was no detectable effect of chronic AF on miR expression in LA tissue, but miR expression in RA was strongly influenced by AF, with 47 miRs showing differential expression. LA volume correlated with miR expression changes in both LA and RA, but the affected miRs were different for the two atrial groups. Conclusions: VHD and AF influence miR expression patterns in LA and RA, but these are affected differently by disease progression and by the development of AF. These findings provide new insights into the progression of VHD. RA tissue is not a useful surrogate for LA in studies of mitral valve disease. 34 arrays from either the left or right atrium from patients with Valvular Heart Disease (VHD), patients undergoing coronary artery bypass grafting (CABG), or healthy controls. Arrays in this series were generated on V2 and V3 Agilent microRNA arrays and analysed in combination.
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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.
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Project description:To examine biological changes and regionality dictating structural remodelling in Atrial Fibrillation, we performed NanoString GeoMx Digital Spatial Profiling (DSP) of tissue biopsies from AF and SR patients. Regions were selected from adipose tissue and atrail appendage tissue close or far apart from tissue interphase.
2024-07-19 | GSE261363 | GEO
Project description:Background: Chronic atrial fibrillation (AF) is a complication associated with the dilated atria of patients with valvular heart disease and contributes to worsened pathology. Methods and Results: Using microarray technology, we examined microRNA (miR) expression profiles in right and left atrial appendage tissue from valvular heart disease (VHD) patients. Right atrial appendage from patients undergoing coronary artery bypass grafting (CABG) and left atrial (LA) appendage from healthy hearts not used for transplant were used as controls. VHD induced different changes in miR expression in LA compared with right atria (RA). Fifty-two (52) miRs were altered by VHD in LA, compared with 5 in RA tissue. There was no detectable effect of chronic AF on miR expression in LA tissue, but miR expression in RA was strongly influenced by AF, with 47 miRs showing differential expression. LA volume correlated with miR expression changes in both LA and RA, but the affected miRs were different for the two atrial groups. Conclusions: VHD and AF influence miR expression patterns in LA and RA, but these are affected differently by disease progression and by the development of AF. These findings provide new insights into the progression of VHD. RA tissue is not a useful surrogate for LA in studies of mitral valve disease.
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