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Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles

ABSTRACT: Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles

PROVIDER: PRJNA417059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6253440.fastq.gz	Fastqsanger.gz
	SRR6253450.fastq.gz	Fastqsanger.gz
	SRR6253460.fastq.gz	Fastqsanger.gz
	SRR6253441.fastq.gz	Fastqsanger.gz
	SRR6253451.fastq.gz	Fastqsanger.gz

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Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles [wntgof]

Project description:Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles [wntgof]

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Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles [wntlof]

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Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles [wntlof]

Project description:Several inherited arrhythmias primarily affect the right ventricle, including Brugada syndrome and arrhythmogenic cardiomyopathy, however the molecular basis of this chamber predilection is not well understood. Right and left ventricular cardiomyocytes derive from distinct progenitor populations. Here, we show that Hrt2, a gene associated with Brugada syndrome, is a direct target of Wnt signaling in the right ventricle and Notch signaling in the left ventricle. Perturbations of Wnt and Notch signaling during development and in the adult lead to chamber-specific transcriptional effects on Hrt2 expression associated with distinct binding patterns to Hrt2 enhancers. Differential enhancer binding is present at early developmental stages when the signaling pathways are active and persists into adulthood. Consistent with chamber-specific regulation, mice deficient in Wnt transcriptional activity dysregulate only a small fraction of transcripts in common between ventricles. Wnt target gen es important for cellular electrophysiology are differentially regulated, resulting in perturbed cardiac conduction and cellular electrophysiological parameters only within the right ventricle. Ex vivo and in vivo physiologic stimulation of the right ventricle is sufficient to induce ventricular tachycardia in Wnt transcriptionally inactive hearts, while left ventricular stimulation has no effect. Taken together, these data delineate mechanisms underlying ventricular-specific arrhythmia susceptibility due to embryonic programming.

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Differential Wnt-mediated Programming and Arrhythmogenesis in Right versus Left Ventricles [wntgof]

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Left-right transcriptomic differences in adult male mouse heart ventricles

Project description:Left and right heart ventricles of adult male mice were profiled to determine the differences in gene expression, control, coordination and signaling fabrics Two-sides (L= left, R = right) gene expression profiling experiment in adult mouse male (M) ventricles (V). 4 biological replicates: MVL1-4, MVR1-4.

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Left-right transcriptomic differences in adult male mouse heart ventricles

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Differential Wnt-mediated programming and arrhythmogenesis in right versus left ventricles.

Project description:Several inherited arrhythmias, including Brugada syndrome and arrhythmogenic cardiomyopathy, primarily affect the right ventricle and can lead to sudden cardiac death. Among many differences, right and left ventricular cardiomyocytes derive from distinct progenitors, prompting us to investigate how embryonic programming may contribute to chamber-specific conduction and arrhythmia susceptibility. Here, we show that developmental perturbation of Wnt signaling leads to chamber-specific transcriptional regulation of genes important in cardiac conduction that persists into adulthood. Transcriptional profiling of right versus left ventricles in mice deficient in Wnt transcriptional activity reveals global chamber differences, including genes regulating cardiac electrophysiology such as Gja1 and Scn5a. In addition, the transcriptional repressor Hey2, a gene associated with Brugada syndrome, is a direct target of Wnt signaling in the right ventricle only. These transcriptional changes lead to perturbed right ventricular cardiac conduction and cellular excitability. Ex vivo and in vivo stimulation of the right ventricle is sufficient to induce ventricular tachycardia in Wnt transcriptionally inactive hearts, while left ventricular stimulation has no effect. These data show that embryonic perturbation of Wnt signaling in cardiomyocytes leads to right ventricular arrhythmia susceptibility in the adult heart through chamber-specific regulation of genes regulating cellular electrophysiology.

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