作者: Jan Haas , Karen S. Frese , Yoon Jung Park , Andreas Keller , Britta Vogel
关键词: Heart failure 、 Epigenetics 、 DNA methylation 、 Internal medicine 、 Gene 、 Biology 、 Endocrinology 、 Dilated cardiomyopathy 、 Heart disease 、 Cancer research 、 Methylation 、 Lymphocyte antigen 75
摘要: 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 progression DCM, either by genetic or epigenetic factors may interact with environmental stimuli. In present study, we examined genome-wide cardiac DNA methylation patients idiopathic DCM controls. We detected differences pathways related to heart disease, but also genes yet unknown function failure, namely Lymphocyte antigen 75 (LY75), Tyrosine kinase-type cell surface receptor HER3 (ERBB3), Homeobox B13 (HOXB13) Adenosine A2A (ADORA2A). Mass-spectrometric analysis bisulphite-sequencing enabled confirmation observed changes independent cohorts. Aberrant was associated significant LY75 ADORA2A mRNA expression, not ERBB3 HOXB13. vivo studies orthologous ly75 adora2a zebrafish demonstrate a functional role these adaptive maladaptive failure.