Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation
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ABSTRACT:
PROVIDER: PRJNA369836 | ENA |
REPOSITORIES: ENA
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Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation [RNA-seq]
| PRJNA413070 | ENA
Project description:Comparison of total RNA of atrial and ventricular chambers from adult zebrafish heart. The goal was to identify chamber specific transcripts and atrial enriched transcripts that can be linked to atrial or ventricular septal defects in mammals.
2018-05-09 | GSE94490 | GEO
Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation II
| PRJNA371293 | ENA
Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation I
| PRJNA371294 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-05-09 | GSE94492 | GEO
Project description:For the study of possible downstream targets of Meis2b, we compared the following expression profiles: 48hpf whole larvae of meis2bs988/s988 to meis2b+/+ siblings, whole heart of 3 wpf meis2bs988/s988 to meis2b+/s988 siblings, atria of 3 mpf meis2bs988/s988 to meis2bs988/+ siblings, and ventricle to atrium of 3 mpf WT zebrafish.
2018-05-09 | GSE94491 | GEO
Project description:Comparison of the meis2b+ and the meis2b- halves of the atrium of the adult zebrafish atrium reveals the existence of two different transcriptional domains. These two domains analogous to that of the two atria in terrestrial vertebrates
2018-05-09 | GSE104573 | GEO
Project description:We analyzed data from sequencing-based massively parallel reporter assays (MPRAs) retaining the strand orientation of the alignments. These analyses showed pervasive asymmetry in reporter signal from test element strand orientation. Present in elements derived from all regions of the human genome, we found test elements derived from gene bodies display concordant strand asymmetry with the sense orientation of the gene body. Furthermore, we observe that test elements form Alu sequence also present concordant strand asymmetry with Alu retrotransposon features. We establish sequence features that drive some of this asymmetry.
2020-12-04 | GSE156857 | GEO
Project description:Obscurins are giant, modular, cytoskeletal proteins that regulate striated muscle structure and function. Immunoglobulin domains 58/59 (Ig58/59) of obscurin interact with diverse proteins including titin variants and phospholamban. Mutations within Ig58/59 that alter these binding interactions have been linked to the development of myopathy in humans, underscoring the pathophysiological significance of this module. We previously generated a constitutive deletion mouse model, Obscn-ΔIg58/59, that expresses obscurin lacking Ig58/59 and comprehensively characterized the effects of this deletion on cardiac morphology and function through aging. Our findings demonstrated that Obscn-ΔIg58/59 male animals develop severe arrhythmia characterized by spontaneous atrial fibrillation/junctional escape by 6-months of age, with atrial enlargement and ventricular remodeling manifesting by 12-months. Herein, we aim to mechanistically evaluate the impact of the Ig58/59 deletion in atria at the cellular level and determine the molecular basis for atrial enlargement and arrhythmia due to the physiological process of aging. Ultrastructural evaluation of sedentary aging male Obscn-ΔIg58/59 atria revealed prominent Z-disk streaming and misalignment. More importantly, Obscn-ΔIg58/59 atrial cardiomyocytes exhibited increased Ca2+ spark frequency and age-specific alterations in Ca2+ cycling kinetics and sarcoplasmic reticulum Ca2+ content that preceded those observed in Obscn-ΔIg58/59 ventricular cardiomyocytes. Proteomic and phospho-proteomic analyses revealed extensive and novel alterations in the expression and phosphorylation profile of major cytoskeletal proteins, Ca2+ regulators, and Z-disk associated protein complexes in Obscn-ΔIg58/59 atria through aging that likely underlie the observed atrial pathologies. These studies are the first to evaluate the role of obscurin in atria and to reveal chamber-specific molecular alterations due to Ig58/59 deletion. Moreover, our findings provide new molecular insights into a genetic model of spontaneous atrial fibrillation and remodeling where atrial dysfunction precedes ventricular maladaptation.
2023-04-11 | PXD028904 | Pride
Project description:Background Atrial fibrosis plays a critical role in the development of atrial fibrillation (AF). Exosome is a promising cell-free therapeutic approach for the treatment of AF. The purpose of this study was to explore the mechanisms underlying exosomes derived from atrial myocytes regulated atrial remodeling and ask whether their manipulation allows for therapeutic modulation of fibrosis potential abnormalities during AF. Methods We isolated exosomes from atrial myocytes and patients serum, microRNA (miRNA) sequencing analyzed the exosomal miRNAs in atrial myocytes-exosomes and patients serum-exosomes. mRNA sequencing and bioinformatics analysis corroborate the key gene as direct targets of miR-210-3p. Results The miRNAs sequencing analysis identified that miR-210-3p expression significantly increased in exosomes of tachypacing atrial myocytes and serum of AF patients. In vitro, the analysis showed that miR-210-3p inhibitor reversed tachypacing-induced proliferation and collagen synthesis in atrial fibroblasts. Accordingly, KO miR-210-3p could reduce the incidence of AF and ameliorate atrial fibrosis induced by Ang Ⅱ. The mRNA sequencing analysis and Dual-Luciferase reporter assay proved that glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is the potential target gene of miR-210-3p. The functional analysis suggests that GPD1L regulated atrial fibrosis via PI3K/AKT signaling pathway. Besides, silencing GPD1L in atrial fibroblasts induced cells proliferation and these effects could be reversed by PI3K inhibitor (LY294002). Conclusion We demonstrate that atrial myocytes-derived exosomal miR-210-3p promoted the proliferation and collagen synthesis via inhibiting GPD1L in atrial fibroblasts. Preventing pathological crosstalk between atrial myocytes and fibroblasts may be as a novel target to improve atrial fibrosis in AF.
2022-08-17 | GSE210894 | GEO