NDLI: H3K9 histone methyltransferase G9a ameliorates dilated cardiomyopathy via the downregulation of cell adhesion molecules.

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H3K9 histone methyltransferase G9a ameliorates dilated cardiomyopathy via the downregulation of cell adhesion molecules.

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H3K9 histone methyltransferase G9a ameliorates dilated cardiomyopathy via the downregulation of cell adhesion molecules.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chen, Guiying Wang, Xu Zhang, Yina Tian, Ye Ru, Xiaoxue Zhou, Lijun
Description	Author Affiliation: Chen G ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Wang X ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Zhang Y ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Ru X ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Zhou L ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Tian Y ( Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.)
Abstract	Dilated cardiomyopathy (DCM) is one of the leading causes of mortality; however, the underlying molecular mechanisms of DCM remain to be elucidated. H3K9 histone methyltransferase G9a has been previously characterized, although its functions in DCM are not yet understood. Cell adhesion molecules (CAM) are highly expressed in diseased human hearts and were thought to contribute to chronic degeneration in cardiac incompetence; however, it has been suggested that G9a may suppress the effects of CAM. The aim of the present study was to investigate whether G9a decreased the risk of DCM via regulation of CAM expression. A rat model of DCM was induced using furazolidone (FZ) treatment and numerous parameters were examined. G9a RNA interference (RNAi) was applied to primary neonatal cardiomyocytes (PNCs). Reverse transcription quantitative polymerase chain reaction and western blot analyses were used to examine the expression levels of G9a in the DCM model and PNCs. The growth rate of PNCs was evaluated following G9a RNAi and FZ treatment. The results confirmed that the expression levels of G9a were significantly decreased in the DCM model compared with those in the control group (P<0.01). Conversely, CAM expression levels were significantly increased in the DCM model compared with those in the control group (P<0.01). In PNCs, the expression of CAM was upregulated following G9a silencing using RNAi. Following threeday culture, the growth rate of PNCs was inhibited by 70 and 35% following FZ treatment and G9a RNAi, respectively. In conclusion, G9a ameliorated DCM via downregulation of CAMs, therefore indicating its potential for use in the treatment of DCM.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Cardiomyopathy, Dilated Metabolism Cell Adhesion Molecules Genetics Gene Expression Regulation Histone-lysine N-methyltransferase Animals Physiopathology Disease Models, Animal Down-regulation Myocytes, Cardiac Rna Interference Rna, Messenger Rna, Small Interfering Ventricular Remodeling Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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