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

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 three‑day 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.