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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 [ChIP-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

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

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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.

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Abnormalities of cellular polarity underlie the primary substrate in a genetic form of atrial fibrillation

Project description:Atrial fibrillation (AF) is the most common clinical arrhythmia and is associated with heart failure and stroke. The primary substrate for AF is poorly understood due to limited access to primary human tissue and the lack of mechanistically faithful in vitro or in vivo models. We used an MYH6:mCherry knock-in reporter line to generate and purify human pluripotent stem cell-derived cardiomyocytes displaying electrophysiological and molecular characteristics of atrial cells (hPSC-atrial cells). We modeled human MYL4 mutants, one of the few definitive genetic causes of AF. Single cell transcriptomics on hPSC-atrial cells (WT and MYL4 mutant) was performed to study changes in gene expression among the cell types that exist in atrial lineage.

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