Long noncoding RNA myocardial infarction-associated transcript is associated with the microRNA-150-5p/P300 pathway in cardiac hypertrophy

In numerous diseases, abnormal expression of myocardial infarction-associated transcript (MIAT) has been reported to be involved in cell proliferation, apoptosis and migration. However, whether this long non-coding RNA MIAT has a regulatory effect on heart hypertrophy requires further investigation. To this end, the present study evaluated MIAT in hypertrophic cardiomyocytes in vitro and in vivo. Neonatal rat ventricular myocytes (NRVMs) were induced by isoproterenol (ISO) to create a cell hypertrophy model, and mice were intraperitoneally injected with ISO to establish an animal model. Echocardiography, immunofluorescence staining, western blot analysis, RNA isolation and reverse transcription-polymerase chain reaction were applied to test the involvement of MIAT in cardiac hypertrophy. The results revealed that MIAT was upregulated under ISO stimulation at the mRNA level both in vivo and in vitro. Silencing of MIAT resulted in decreased expression levels of atrial natriuretic peptide and brain natriuretic peptide in ISO-treated NRVM cardiomyocytes, confirming the connection between MIAT and hypertrophy. Furthermore, MIAT small interfering RNA significantly increased microRNA (miR)-150 and decreased P300 expression in NRVMs. In conclusion, the MIAT/miR-150-5p axis targets P300 as a positive regulator of cardiomyocyte hypertrophy.