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Reprogramming of three-dimensional chromatin architecture drives human dilated cardiomyopathy

ABSTRACT: Reprogramming of three-dimensional chromatin architecture drives human dilated cardiomyopathy

PROVIDER: PRJNA694042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13506000_1.fastq.gz	Fastqsanger.gz
	SRR13506000_2.fastq.gz	Fastqsanger.gz
	SRR13506100_1.fastq.gz	Fastqsanger.gz
	SRR13506100_2.fastq.gz	Fastqsanger.gz
	SRR13506001_1.fastq.gz	Fastqsanger.gz

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Reprogramming of three-dimensional chromatin architecture drives human dilated cardiomyopathy

Project description:Here we generated the first reference 3D chromatin contact maps from 101 biobanked human heart tissue samples through HiChIP (H3K27ac), in situ Hi-C, ChIP-seq, ATAC-seq and RNA-seq profiling. We discovered that the active regulatory elements and their connectome were extensively reprogrammed in DCM and contributed to transcription dysregulation implicated for DCM development. Higher-order chromatin structures indicated that the overall genome architecture was largely invariant in DCM and chromatin accessibility did not alter DCM-specific H3K27ac loops. This provided insight to the mechanistic hierarchies between higher-order chromatin structures, cis-regulatory elements and differential chromatin accessibilities in DCM, suggesting the importance of sequence-specific transcription factors. Intriguingly, we uncovered that the DCM-specific H3K27ac loops anchors exhibited a strong enrichment for Heart And Neural Crest Derivatives Expressed 1 (HAND1), a key transcription factor involved in early cardiogenesis. In line with this, its protein expression was upregulated in human DCM hearts and mouse failing hearts. Functional analyses by ectopic overexpression of HAND1 in human iPSC-derived cardiomyocytes induced cell hypertrophy and abnormal electrophysiology. Moreover, cardiomyocyte-specific overexpression of HAND1 in the mouse heart resulted in cardiomyocyte enlargement, increased heart weight/body weight ratio and dilated left ventricle. Echocardiography showed that cardiomyocyte-specific Hand1 overexpression in the mouse heart led to cardiac dysfunction and remodeling. Thus, aberrant activation of HAND1 in adult cardiomyocytes recapitulated the phenotypes observed in human DCM and indicated the involvement of a partial reactivation of a developmentally earlier cell identity program in the disease.

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