MicroRNA-150 aggravates H2O2-induced cardiac myocyte injury by down-regulating c-myb gene

MicroRNAs （miRNAs） are one class of non-coding RNAs that play an important role in post-transcriptional regula- tion v/a the degradation or translational inhibition of their target genes. MicroRNA-150 （miR-150） plays a vital role in regulating the development of B and T lymphocytes. Although the dysregulation of miR-150 was confirmed in human myocardial infarction, little is known regarding the biological functions of miR-150 in response to reactive oxygen species （ROS）-mediated gene regulation in cardiac myocytes. Using quantitative real-time reverse transcrip- tion-polymerase chain reaction, we demonstrated that the level of miR-150 was up-regulated in cardiac myocytes after treatment with hydrogen peroxide （H2O2）. To identify the potential roles of miR-150 in H2O2-mediated gene regula- tion, we modulated expression of miR-150 using miR-150 in- hibitor and miR-150 mimics. Results showed that silencing expression of miR-150 decreased H2O2-induced cardiac cell death and apoptosis. In lymphocytes, c-myb was a direct target of miR-150. In cardiac myocytes, we found that c-myb was also involved in miR-150-mediated H2O2-induced cardiac cell death. These results suggested that miR-150 par- ticipates in H2O2-mediated gene regulation and functional modulation in cardiac myocytes. MiR-150 may play an essential role in heart diseases related to ROS, such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury.