RBM15 Protects Cardiomyocytes Apoptosis under Myocardial Infarction Through Stabilizing NAE1

RNA bind proteins (RBP) play multiple roles in several biological processes. However, RBM15, not only as an important RBP but also as a significant regulator in RNA methylation, its roles in cardiovascular diseases are still elusive. This study aims to investigate the biological function of RBM15 and its fundamental mechanisms in myocardial infarction (MI). MeRIP-seq was used to explore the m6A difference between MI and normal tissues. Our findings showed the elevated level of m6A in MI and its transcription profile in both MI and normal tissues. RBM15 is a main regulator and its overexpression attenuates apoptosis in cardiomyocytes and improves cardiac function in mice after MI. Then, we used one target NAE1 and its inhibitor (MLN4924) to investigate the impact of RBM15 targets on cardiomyocytes. Finally, enhanced m6A methylation in the presence of RBM15 overexpression can lead to the increased expression and stability of NAE1. Our findings suggest enhanced m6A level is a protective mechanism in MI and RBM15 is significantly upregulated in MI and promotes cardiac function. This study is the first to show RBM15 affected MI by stabilizing its target on the cell apoptosis function, which might provide a new sight into MI therapy.