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ABSTRACT: Background
Cardiovascular disease is associated with epigenomic changes in the heart; however, the endogenous structure of cardiac myocyte chromatin has never been determined.Methods
To investigate the mechanisms of epigenomic function in the heart, genome-wide chromatin conformation capture (Hi-C) and DNA sequencing were performed in adult cardiac myocytes following development of pressure overload-induced hypertrophy. Mice with cardiac-specific deletion of CTCF (a ubiquitous chromatin structural protein) were generated to explore the role of this protein in chromatin structure and cardiac phenotype. Transcriptome analyses by RNA-seq were conducted as a functional readout of the epigenomic structural changes.Results
Depletion of CTCF was sufficient to induce heart
SUBMITTER: Rosa-Garrido M
PROVIDER: S-EPMC5648689 | biostudies-literature | 2017 Oct
REPOSITORIES: biostudies-literature