Gene expression in rabbit left atrial free wall and left atrial appendage
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ABSTRACT:
PROVIDER: PRJNA483207 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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:Regional differential expression of atrial fibrillation risk genes in the left atrium and pulmonary veins is not well studied, but may yield insights into atrial fibrillation pathogenesis. We tested the hypothesis that there is significant regional differential expression in left atrium structures. RNAseq was performed in 25 regions within the pulmonary veins (n=12), left atrial body (n=10), and left atrial appendage (n=3) from a 75 year old male with hypertension and atrial fibrillation who died of a stroke. These data show that genes involved in atrial fibrillation pathogenesis have substantial regional expression heterogeneity, particularly when comparing the left atrial body, pulmonary veins and left atrial appendage.
2020-11-14 | GSE161450 | GEO
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.
2011-12-21 | E-GEOD-28954 | 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.
2011-12-21 | GSE28954 | GEO
Project description:Adult rabbit left ventricle RNAseq
| PRJNA475561 | ENA
Project description:The left atrium consists of three major parts: the peri-pulmonary vein portion, the appendage, and the vestibule. Previous transcriptional profiling of the adult left atrium and identification of the Tbx5-dependent transcriptome has focused on the atrial appendage (Nadadur et al 2016, Science Translational Medicine). In that study, Tbx5 was shown to regulate a gene regulatory network of atrial identity in the appendage and in its absence results in atrial fibrillation. In order to investigate the regional differences in the transcriptome of the left atrium, the left atrial appendage and the peri-pulmonary vein portion from adult mice were compared by RNA-sequencing. Additionally, as Tbx5 is major regulator of atrial identity, the peri-pulmonary vein portion of the atria was likewise examined following removal of Tbx5 using an adult specific conditional knockout of Tbx5.
2020-03-10 | GSE128870 | GEO
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.
2016-08-09 | GSE79768 | GEO
Project description:The developmental origin of the c-kit expressing progenitor cell pool in the adult heart has remained elusive. Recently, it has been discovered that the injured heart is enriched with c-kit+ cells, which also express the hematopoietic marker CD45. In this study, we characterize the phenotype and transcriptome of the c-kit+/CD45+ cell population, originating from the left atrial appendage. These cells are defined as cardiac macrophage progenitors. We also demonstrate that the c-kit+/CD45+ progenitor cell population activates heart development, neural crest and pluripotency associated pathways in vitro, in conjunction with CD45 down-regulation, and acquire a c-kit+/lin- phenotype. This spontaneous reprogramming progresses further to a highly proliferative, partially myogenic phenotype. Our data suggests that c-kit+/lin- cells and cardiac macrophages have a common lineage origin possibly resolving some current conundrums in the field of cardiac regeneration. Two different stem cell types were grown by altering the tissue digestion protocol. To investigate their transcriptional profiles we prepared RNA from two cell sorted replicates per cell type and from two left ventricular biopsy samples as controls.
2016-07-03 | E-GEOD-57064 | biostudies-arrayexpress