Open AccessDNA methylation dysregulations in valvular atrial fibrillation
Author(s) -
Shen Kangjun,
Tu Tao,
Yuan Zhaoshun,
Yi Jiangfeng,
Zhou Yangzhao,
Liao Xiaobo,
Liu Qiming,
Zhou Xinmin
Publication year - 2017
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.22715
Subject(s) - dna methylation , methylation , medicine , epigenetics , pathogenesis , atrial fibrillation , methyltransferase , promoter , gene , gene expression , microbiology and biotechnology , biology , genetics
Background The epigenetic changes underlying the development of atrial fibrillation ( AF ) remain incompletely understood. Limited evidence suggests that abnormal DNA methylation might be involved in the pathogenesis of AF . In the present study, we evaluated the methylation status of genomic DNA from myocardial tissue in AF patients and sinus rhythm ( SR ) patients systematically. Hypothesis DNA methylation dysregulations will be associated with valvular AF . Methods Right atrial myocardial tissue was obtained from rheumatic valvular patients who had undergone valve replacement surgery ( SR group, n = 10; AF group, n = 10). The global DNA methylation level, the promoter methylation level of the natriuretic peptide receptor‐A gene ( NPRA ), and its correlation with the mRNA expression level of DNA methyltransferase genes were detected. Results The global DNA methylation level was significantly higher in the AF group than in the SR group ( P < 0.05). The NPRA mRNA expression was decreased and the NPRA gene was hypermethylated in the AF group ( P < 0.05). Meanwhile, the NPRA mRNA expression level has a negative correlation with the mean methylation level in the promoter region of the NPRA gene. Conclusions DNA methylation dysregulations may be relevant in the pathogenesis of AF . DNA methyltransferase 3B likely plays an essential role in the DNA methylation dysregulations in AF .