The role of stromal and immune cells in atrial disease
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ABSTRACT:
PROVIDER: PRJNA933179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18151700.fastq.gz | Fastqsanger.gz | |||
| SRR18151701.fastq.gz | Fastqsanger.gz | |||
| SRR18151702.fastq.gz | Fastqsanger.gz | |||
| SRR18151703.fastq.gz | Fastqsanger.gz | |||
| SRR18151704.fastq.gz | Fastqsanger.gz |
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Project description:In atrial fibrillation, disturbed electrical conduction disrupts the coordinated contraction of the heart’s antechambers, increasing the risk of stroke and heart failure. The rising prevalence of this disease approaches 9% in patients >65 years. Studying freshly isolated human atrial tissue and a new mouse model, we here decipher how immune and stromal cells contribute to the structural tissue remodeling that underlies atrial fibrillation. Single-cell transcriptomes from control and diseased human atria documented macrophage doubling at the expense of endothelial and mural cells. An inflammatory monocyte and a pro-fibrotic SPP1+ macrophage cluster expanded in patients with atrial fibrillation. To experimentally perturb pathways observed in patients, we matched their risk factors Hypertension, Obesity and Mitral valvE Regurgitation (HOMER) in mice. Atrial single-cell transcriptomes obtained in HOMER mice, which developed enlarged, fibrillation-prone atria, recapitulated human cell composition and transcriptome variations. Recruitment drove the expansion of atrial macrophages; accordingly, inhibition of monocyte migration reduced arrhythmia in Ccr2-/- HOMER mice. Deleting Spp1 established macrophage-derived osteopontin as a pleiotropic signal that promotes atrial fibrillation through pro-fibrotic, inflammatory crosstalk with an arsenal of local immune and stromal cells. Taken together, we identify SPP1+ macrophages as targets for immunomodulatory therapy in atrial fibrillation.
2023-07-13 | GSE224947 | GEO
Project description:In atrial fibrillation, disturbed electrical conduction disrupts the coordinated contraction of the heart’s antechambers, increasing the risk of stroke and heart failure. The rising prevalence of this disease approaches 9% in patients >65 years. Studying freshly isolated human atrial tissue and a new mouse model, we here decipher how immune and stromal cells contribute to the structural tissue remodeling that underlies atrial fibrillation. Single-cell transcriptomes from control and diseased human atria documented macrophage doubling at the expense of endothelial and mural cells. An inflammatory monocyte and a pro-fibrotic SPP1+ macrophage cluster expanded in patients with atrial fibrillation. To experimentally perturb pathways observed in patients, we matched their risk factors Hypertension, Obesity and Mitral valvE Regurgitation (HOMER) in mice. Atrial single-cell transcriptomes obtained in HOMER mice, which developed enlarged, fibrillation-prone atria, recapitulated human cell composition and transcriptome variations. Recruitment drove the expansion of atrial macrophages; accordingly, inhibition of monocyte migration reduced arrhythmia in Ccr2-/- HOMER mice. Deleting Spp1 established macrophage-derived osteopontin as a pleiotropic signal that promotes atrial fibrillation through pro-fibrotic, inflammatory crosstalk with an arsenal of local immune and stromal cells. Taken together, we identify SPP1+ macrophages as targets for immunomodulatory therapy in atrial fibrillation.
2023-07-13 | GSE225671 | GEO
Project description:In atrial fibrillation, disturbed electrical conduction disrupts the coordinated contraction of the heart’s antechambers, increasing the risk of stroke and heart failure. The rising prevalence of this disease approaches 9% in patients >65 years. Studying freshly isolated human atrial tissue and a new mouse model, we here decipher how immune and stromal cells contribute to the structural tissue remodeling that underlies atrial fibrillation. Single-cell transcriptomes from control and diseased human atria documented macrophage doubling at the expense of endothelial and mural cells. An inflammatory monocyte and a pro-fibrotic SPP1+ macrophage cluster expanded in patients with atrial fibrillation. To experimentally perturb pathways observed in patients, we matched their risk factors Hypertension, Obesity and Mitral valvE Regurgitation (HOMER) in mice. Atrial single-cell transcriptomes obtained in HOMER mice, which developed enlarged, fibrillation-prone atria, recapitulated human cell composition and transcriptome variations. Recruitment drove the expansion of atrial macrophages; accordingly, inhibition of monocyte migration reduced arrhythmia in Ccr2-/- HOMER mice. Deleting Spp1 established macrophage-derived osteopontin as a pleiotropic signal that promotes atrial fibrillation through pro-fibrotic, inflammatory crosstalk with an arsenal of local immune and stromal cells. Taken together, we identify SPP1+ macrophages as targets for immunomodulatory therapy in atrial fibrillation.
2023-07-13 | GSE197518 | 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
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2023-07-13 | GSE224959 | GEO
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
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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