Alterations in cardiac DNA methylation in human dilated cardiomyopathy. Haas, J., Frese, K. S, Park, Y. J., Keller, A., Vogel, B., Lindroth, A. M, Weichenhan, D., Franke, J., Fischer, S., Bauer, A., Marquart, S., Sedaghat-Hamedani, F., Kayvanpour, E., Köhler, D., Wolf, N. M, Hassel, S., Nietsch, R., Wieland, T., Ehlermann, P., Schultz, J., Dösch, A., Mereles, D., Hardt, S., Backs, J., Hoheisel, J. D, Plass, C., Katus, H. A, & Meder, B. EMBO molecular medicine, 5:413–429, March, 2013. doi abstract bibtex Dilated cardiomyopathies (DCM) show remarkable variability in their age of onset, phenotypic presentation, and clinical course. Hence, disease mechanisms must exist that modify the occurrence and progression of DCM, either by genetic or epigenetic factors that may interact with environmental stimuli. In the present study, we examined genome-wide cardiac DNA methylation in patients with idiopathic DCM and controls. We detected methylation differences in pathways related to heart disease, but also in genes with yet unknown function in DCM or heart failure, namely Lymphocyte antigen 75 (LY75), Tyrosine kinase-type cell surface receptor HER3 (ERBB3), Homeobox B13 (HOXB13) and Adenosine receptor A2A (ADORA2A). Mass-spectrometric analysis and bisulphite-sequencing enabled confirmation of the observed DNA methylation changes in independent cohorts. Aberrant DNA methylation in DCM patients was associated with significant changes in LY75 and ADORA2A mRNA expression, but not in ERBB3 and HOXB13. In vivo studies of orthologous ly75 and adora2a in zebrafish demonstrate a functional role of these genes in adaptive or maladaptive pathways in heart failure.
@Article{Haas2013,
author = {Haas, Jan and Frese, Karen S and Park, Yoon Jung and Keller, Andreas and Vogel, Britta and Lindroth, Anders M and Weichenhan, Dieter and Franke, Jennifer and Fischer, Simon and Bauer, Andrea and Marquart, Sabine and Sedaghat-Hamedani, Farbod and Kayvanpour, Elham and Köhler, Doreen and Wolf, Nadine M and Hassel, Sarah and Nietsch, Rouven and Wieland, Thomas and Ehlermann, Philipp and Schultz, Jobst-Hendrik and Dösch, Andreas and Mereles, Derliz and Hardt, Stefan and Backs, Johannes and Hoheisel, Jörg D and Plass, Christoph and Katus, Hugo A and Meder, Benjamin},
title = {Alterations in cardiac DNA methylation in human dilated cardiomyopathy.},
journal = {EMBO molecular medicine},
year = {2013},
volume = {5},
pages = {413--429},
month = mar,
issn = {1757-4684},
abstract = {Dilated cardiomyopathies (DCM) show remarkable variability in their age of onset, phenotypic presentation, and clinical course. Hence, disease mechanisms must exist that modify the occurrence and progression of DCM, either by genetic or epigenetic factors that may interact with environmental stimuli. In the present study, we examined genome-wide cardiac DNA methylation in patients with idiopathic DCM and controls. We detected methylation differences in pathways related to heart disease, but also in genes with yet unknown function in DCM or heart failure, namely Lymphocyte antigen 75 (LY75), Tyrosine kinase-type cell surface receptor HER3 (ERBB3), Homeobox B13 (HOXB13) and Adenosine receptor A2A (ADORA2A). Mass-spectrometric analysis and bisulphite-sequencing enabled confirmation of the observed DNA methylation changes in independent cohorts. Aberrant DNA methylation in DCM patients was associated with significant changes in LY75 and ADORA2A mRNA expression, but not in ERBB3 and HOXB13. In vivo studies of orthologous ly75 and adora2a in zebrafish demonstrate a functional role of these genes in adaptive or maladaptive pathways in heart failure.},
chemicals = {Antigens, CD, DEC-205 receptor, Lectins, C-Type, Minor Histocompatibility Antigens, RNA, Messenger, Receptor, Adenosine A2A, Receptors, Cell Surface, Zebrafish Proteins},
citation-subset = {IM},
completed = {2013-07-22},
country = {England},
doi = {10.1002/emmm.201201553},
issn-linking = {1757-4676},
issue = {3},
keywords = {Adult; Aged; Animals; Antigens, CD, genetics, metabolism; Biopsy; Cardiomyopathy, Dilated, genetics, metabolism, physiopathology; Case-Control Studies; Cluster Analysis; DNA Methylation; Epigenesis, Genetic; Female; Gene Expression Regulation; Gene Knockdown Techniques; Genetic Predisposition to Disease; HEK293 Cells; Humans; Lectins, C-Type, genetics, metabolism; Male; Mass Spectrometry; Middle Aged; Minor Histocompatibility Antigens; Molecular Sequence Data; Myocardium, metabolism; Phenotype; RNA, Messenger, metabolism; Rats; Receptor, Adenosine A2A, genetics, metabolism; Receptors, Cell Surface, genetics, metabolism; Reproducibility of Results; Sequence Analysis, DNA, methods; Sequence Analysis, Protein; Transfection; Zebrafish, genetics, metabolism; Zebrafish Proteins, genetics, metabolism},
nlm-id = {101487380},
owner = {NLM},
pmc = {PMC3598081},
pmid = {23341106},
pubmodel = {Print-Electronic},
pubstatus = {ppublish},
revised = {2016-11-25},
}
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