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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ncRNA-Seq]

ABSTRACT: The transcription factor FOG2 (ZFPM2) is upregulated in human heart failure and increased FOG2 expression causes heart failure in mice. We found that FOG2 directly intersects a gene regulatory network driven by the atrial-enriched TF TBX5 and required for atrial cardiomyocyte rhythm control gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE198786 | GEO | 2024/05/02

REPOSITORIES: GEO

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [RNA-Seq]

Project description:The transcription factor FOG2 (ZFPM2) is upregulated in human heart failure and increased FOG2 expression causes heart failure in mice. We found that FOG2 directly intersects a gene regulatory network driven by the atrial-enriched TF TBX5 and required for atrial cardiomyocyte rhythm control gene expression

2024-05-02 | GSE198734 | GEO

FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ChIP-Seq]

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk

Project description:FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [RNA-Seq]

Project description:FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [RNA-Seq]

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ChIP-Seq]

Project description:FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ChIP-Seq]

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ncRNA-Seq]

Project description:FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ncRNA-Seq]

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Project description:The aim of this study was to identify a blood gene expression profile that predicts atrial fibrillation in heart failure patients

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Project description:Atrial fibrillation (AF) remains challenging to prevent and treat. It is associated with increased rates of heart failure, stroke and neurological decline. A key feature of AF is atrial enlargement. However, not all atrial enlargement progresses to pathology and AF. In the current study, we characterized mouse atria from a 1) pathological model (cardiac-specific transgenic (Tg) that develops dilated cardiomyopathy [DCM] and AF due to reduced protective signalling [PI3K]; DCM-dnPI3K), and a 2) physiological model (cardiac-specific Tg with an enlarged heart due to increased insulin-like growth factor 1 receptor; IGF1R). Atrial enlargement in the DCM-dnPI3K Tg, but not IGF1R Tg, was associated with atrial dysfunction, fibrosis and a heart failure gene expression pattern. Proteomics analysis identified proteins and pathways that were differentially regulated in pathological and physiological atrial enlargement, and provides a resource to study potential drug targets for AF.

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Project description:Atrial fibrillation (AF) is the most common sustained arrhythmia with increased risk of stroke and congestive heart failure. AF is a highly genetic heterogeneous disease, but a large proportion of AF cannot be explained by genetic variants only. Some risk factors of AF, tendentious heritable phenomenon, potentially reversible conditions and some subtypes without DNA sequence variation all indicate the participation of DNA methylation in the pathogenesis of AF. Bisulphite converted DNA from the 11 left atrium samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip GPL13534

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Project description:MHCaCre induced knockout of Fog2flox. Aberrant transcriptional regulation contributes to the pathogenesis of both congenital and adult forms of heart disease. While the transcriptional regulator FOG2 is known to be essential for heart morphogenesis and coronary development, its tissue specific function has not been previously investigated. Additionally, little is known about the role of FOG2 in the adult heart. Here we use spatiotemporally regulated inactivation of Fog2 to delineate its function both in embryo and adult heart. Early cardiomyocyte-restricted loss of Fog2 recapitulated the cardiac and coronary defects of the Fog2 germline knockouts. Later cardiomyocyte-restricted loss of Fog2 (Fog2MC) did not result in defects in cardiac structure or coronary vessel formation. However, Fog2MC adult mice had severely depressed ventricular function and died at 8-14 weeks. Fog2MC adult hearts displayed a paucity of coronary vessels. This was associated with myocardial hypoxia, increased cardiomyocyte apoptosis, and cardiac fibrosis. Induced inactivation of Fog2 in adult heart resulted in similar phenotype, as did ablation of FOG2 interaction with the transcription factor GATA4. Loss of FOG2 or FOG2-GATA4 interaction altered expression of a panel of angiogenesis-related genes. Collectively, our data indicated that FOG2 regulates adult heart function and coronary angiogenesis.

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